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Episodic memory in normal aging and Alzheimer disease: Insights from imaging and behavioral studies
Accepted Manuscript Title: Episodic memory in normal aging and Alzheimer Disease: Insights from imaging and behavioral studies Author: Tromp D Bernard F Dufour A Lithfous S Pebayle T Despr´es O PII: DOI: Reference:
S1568-1637(15)30019-2 http://dx.doi.org/doi:10.1016/j.arr.2015.08.006 ARR 604
To appear in:
Ageing Research Reviews
Received date: Accepted date:
23-6-2015 20-8-2015
Please cite this article as: Tromp, D, Bernard, F, Dufour, A, Lithfous, S, Pebayle, T, Despr´es, O, Episodic memory in normal aging and Alzheimer Disease: Insights from imaging and behavioral studies.Ageing Research Reviews http://dx.doi.org/10.1016/j.arr.2015.08.006 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.
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Episodic memory in normal aging and Alzheimer Disease:
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Insights from imaging and behavioral studies
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Tromp Da, Bernard Fa,Dufour Aa,b, Lithfous Sa, Pebayle Tb and Després Oa
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a: Laboratoire de Neurosciences Cognitives et Adaptatives (LNCA - UMR 7364 - CNRS/UDS) - 21 rue
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Becquerel, 67087, Strasbourg. France - [email protected]
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b: Centre d'Investigations Neurocognitives et Neurophysiologiques (CI2N - UMS 3489 - CNRS/UDS) - 21
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rue Becquerel, 67087, Strasbourg. France
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Corresponding author:
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TROMP Delphine
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21 rue Becquerel
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67087 Strasbourg Cedex
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FRANCE
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Tel: +33 (0)3 88 10 67 66
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Fax: +33 (0) 388.106.245
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E-mail: [email protected]
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1/ Introduction .................................................................................................................................................. 5
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2/ Episodic memory processes and cerebral substrates ....................................................................................... 7
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2.1/ Encoding ............................................................................................................................................... 8
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2.2/ Consolidation or storage......................................................................................................................... 9
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2.3/ Retrieval .............................................................................................................................................. 10
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3/ Behavioral data and models clarifying the memory decline performance in normal aging ............................. 12
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4/ Chemical and anatomical data: role of brain imaging study in healthy elderly .............................................. 15
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4.1/ Depletion of neurotransmitters ............................................................................................................. 15
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4.2/ Prefrontal cortex .................................................................................................................................. 17
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4.3/ From HERA to HAROLD: the compensation models ........................................................................... 17
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4.4/ Aging in the PFC: link with behavioral data ......................................................................................... 20
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4.5/ Medial temporal lobes .......................................................................................................................... 21
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4.6/ Are other neural substrates of EM affected by age? ............................................................................... 24
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5/ Inter-individual variability associated with EM in normal aging and Alzheimer disease................................ 26
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5.1/ Lifestyle .............................................................................................................................................. 26
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5.2/ Genetics............................................................................................................................................... 27
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6/ Episodic memory and Alzheimer disease ..................................................................................................... 30
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6.1/ Pathophysiology and characteristics of the disease ................................................................................ 30
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6.2/ Behavioral data .................................................................................................................................... 31
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6.3/ Neural structures implicated in EM declines ......................................................................................... 33
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7/ Conclusion and perspectives........................................................................................................................ 36
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Highlights
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Episodic memory is sensitive to the effects of age and very disrupted in Alzheimer’s disease. It is the first memory system to decline in both normal and pathological aging.
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Neuroimaging studies have been fundamental in distinguishing between normal aging and AD: they
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have shown a particular pattern of morphological and functional distinct brain damage. The prefrontal
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cortex seems to be affected first in non-demented adults whereas the hippocampus is the primary
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structural disorder in this neurological disease.
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Interindividualvariabilities observed during episodic memory performances could be due to several factors including lifestyle and genetic factors.
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Additional or different neurocognitive processes seem to develop both in normal and pathological brains to offset the deficit of episodic memory.
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Abstract
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Age-related cognitive changes often include difficulties in retrieving memories, particularly those that rely on
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personal experiences within their temporal and spatial contexts (i.e., episodic memories).This decline mayvary
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depending on the studied phase (i.e., encoding, storage or retrieval), according to inter-individual differences,
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and whether we are talking about normal or pathological (e.g., Alzheimer disease; AD) aging. Such cognitive
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changesare associated with different structural and functional alterations in the human neural network
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thatunderpins episodic memory. The prefrontal cortex is the first structure to be affected by age, followed by the
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medial temporal lobe (MTL), the parietal cortex and the cerebellum. In AD, however, the modifications occur
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mainly in the MTL (hippocampus and adjacent structures) before spreading to the neocortex. In this review, we
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will present results that attempt to characterize normal and pathological cognitive aging at multiple levels by
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integrating structural, behavioral, inter-individual and neuroimaging measures of episodic memory.
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Keywords: Episodic memory, fMRI, PET, Normal aging, Alzheimer disease
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1/ Introduction
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According to Eurostat (the European Statistical Institute),the proportion of people over 65 years old will
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increase until 2060, when it will reaching 30% of the European population (compared to 16% in 2010). At this
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same time, people over 80 years are predicted to represent 12% of the population (compared to 5% in 2010).
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According to the European Commission’s 2009 Ageing Report, the number of European persons older than 65
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years suffering from at least one disability in activities of daily living will more than double between 2007 and
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2060, reaching 44.4 million by the latter date.This consistent increase inthe aging population will come with
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important health and economic stakes (Freund and Smeeding, 2010; Lutz et al., 2008). We will be challenged to
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allow this aging to occurunder the best possible conditions, and this will need to ‘create a substantial financial
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burden. In 2010, expenses related to the frail elderly (seniors who have lost autonomy) in France were estimated
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to be between 27 and 34 billion euros.
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Normal aging generally induces cognitive impairment, with older people often considered to be less
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efficient than younger people in using memory, attention, visuospatial capacities or executive functions. While
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most aging individuals experience some degree of “normal” cognitive change, the incidence of the
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neurodegenerative diseases collectively classified as “dementia” also increases dramatically with age.Among
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them, alzheimer disease (AD) constitutes the leading cause of dementia in persons aged over 60 years, reaching
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6.7% in subjects 75-79 years old and 31.15% in those over 85 years old (Helmer et al., 2006).
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One of the earliest cognitive changes in aging, and the one that has probably received the most
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attention, is the alteration of memory (Grady, 2008; Park and Gutchess, 2002). Older people exhibit changes in
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the quality of their memories (Friedman et al., 2010; Piolino et al., 2006; Schacter et al., 1997), in
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associationwith difficulties in remembering (Craik and Bialystok, 2006; Davis et al., 2003; Ozen and Rezaki,
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2007). Memory changes are also the most striking cognitive alterations seen in pathological aging, butmemory
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loss in normal aging qualitatively differs from that associated with a diagnosis of AD (for review, see Budson
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and Price, 2005). Major research efforts have focused on trying to distinguish the memory declines attributable
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to normal aging from those that indicate pathological aging, particularly AD(e.g. Ghosh et al., 2011). Such
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studies have shown that we do not have unitary memory; rather, both cross-sectional and longitudinal studies
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have demonstrated that the different memory component systems do not age uniformly, but instead show
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differential vulnerabilities to the effects of aging (Brickman and Stern, 2009).
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The long-term memory (LTM) system is divided into two broad classes: explicit (declarative) memory,
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which requires the conscious recall of information, and implicit (non-declarative) memory, which is based on
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implicit learning (Squire, 1987). Implicit memory includes procedural memory and the Perceptual
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Representation System (PRS),sustainingpriming effects and operant or classical conditioning. In contrast,
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declarative memory is subdivided into semantic memory and episodic memory (EM). Semantic memoryis
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related to general facts and knowledge,whereas EM is a cognitive system that enables an individual to record (or
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encode), store, and retrieve information about personal experiences and the temporal and spatial contexts of
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those experiences (first defined by Tulving, 1972). The classic model of EM refers to both the autobiographical
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recollection of one’s personal past experiences (e.g., What did you eat for breakfast this morning?) and
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laboratory tasks requiring the conscious recognition or recall of experimental materials (e.g., a list of words).
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Although autobiographical memory (AM) has often been equated with EM, it is important to distinguish
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between the two. AM may encompass long periods and is defined by self-related information processing,
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subjective emotional evaluation of memories and a quick, intuitive and pre-conscious feeling of certainty (a
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“feeling of rightness”)to control the veracity and cohesiveness of retrieved memories (Cabeza and St. Jacques,
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2007; Gilboa, 2004; Moscovitch and Winocur, 2002).This memory system consists of episodes recollected from
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an individual’s life based on the combination of episodic (also called episodic autobiographical memory) and
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personal semantic memory (semantic autobiographical memory). In other words, it includes both one’s self-
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knowledgeand the memories that surround this self-knowledge (e.g. Abram et al., 2014; Markowitsch and
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Staniloiu, 2011; Martinelli et al., 2013).Experimental memory, in contrast, is measured in seconds, minutes and
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hours; it is rare and only really considered in cases of psychological and laboratory experiments. Wheeler et al.
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(1997) proposed that,unlike AM, EM requires elaborate, conscious monitoring and awareness to avoid omissions
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and repetitions, and also involvesthe intentional use of retrieval strategies. As AM and its age-related declines
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have already been the subject of many studies and reviews (e.g. Piolino, 2003), the present review will only
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address experimental episodic memory (referred to as EM hereafter).
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The above-described types of memory are all part of the LTM system, where information can remain
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for an infinite time(Glisky, 2007). In contrast, working memory (WM) refers to the active storage and cognitive
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manipulation of information necessary for complex cognitive tasks, in order to achieve an immediate goal (e.g.,
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remembering a phone number). WM is a subcomponent of short-term memory (STM), whichis known to involve
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the passive maintenance of information in the mind over a short period(Cowan, 2008). A classification of the
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different memory systems is presented in Figure 1.
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Aging affects the various memory systems to different degrees, and numerous inter-individual
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differences are seen. While some older adults have significant cognitive deficits, others maintain performances
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equal to those of younger individuals(e.g. Angel et al., 2010; Butler et al., 2004; Shimamura et al., 1995). Some
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systems, such as short-term and procedural memory, do not seem to be affected by normal aging (Brickman and
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Stern, 2009; Craik, 1977; Nilsson, 2003; Zacks et al., 2000). Semantic memory also appears to be immune to
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some of the effects of aging, in that general knowledge and vocabulary are well maintained in older adults (e.g.
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Verhaeghen, 2003; Kennedy et al., 2015).In contrast, EM is highly affected by aging (e.g. Balota et al., 2000;
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Luo and Craig, 2008; McDaniel et al. 2008). This is likely to reflect that EM depends on many processes that are
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underlain by a vast cerebral network. The frontal system, which gives EM a certain consistency by organizing
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information, acts in parallel with the temporal hippocampal system in controlling and organizing the encoding
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and retrieval of EM information via the selection, initiation, elaboration and implementation of relevant
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strategies (Kraemer et al., 2005).Other (far less well studied) structuresare also involved, such as the parietal
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cortex and the cerebellum (the best studied among them), as well as the thalamus and the cingulate gyrus (Wiggs
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et al., 1999; for review, see Cabeza and Nyberg, 2000).Changes at the neuroanatomical, neurophysiological and
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neurochemical levels of the central nervous system are likely to underpin the observed age-related decline in
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EM: decrease in white and gray matters volumes, neuronal numbers and size, reduced efficiency of synaptic
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contacts and decreases in the concentrations of neurotransmitters (Raz, 2000; Burke and Barnes, 2006; Deenis
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and Cabeza, 2008 for a review).All of these changes preferentially affect the frontal brain regions (for review,
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see West, 1996). Post mortem (Meltzer et al., 2003) and in vivo studies haveshown that, compared to the brains
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of young adults, the brains of older adults tend to have lower volumes of gray matter according to an antero-
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posterior gradient (Resnik et al., 2003). Cross-sectional studies suggest that the gray matter volume declines
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steadily across the adult lifespan, whereas the white matter volume increases linearly from birth to young
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adulthood, plateaus during middle age, and declines during old age (Raz et al., 2005). In vivo volumetric studies
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of healthy volunteers have revealed the presence of a significant hippocampal shrinkage (up to 1.18% per year)in
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people in their mid-50s (Lemaître et al., 2005; Raz et al., 2004; Resnick et al., 2000; see also Fjell et al., 2009),
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and to an early and severe atrophy of the prefrontal cortex (PFC) after the age of 20, with an estimated average
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decline of about 5% per decade (Raz and Rodrigue, 2006). On a larger scale, this selective PFC decline observed
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in the elderly (particularly in the dorsolateral PFC; Kraemer et al., 2005) is associated with degradation of the
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executive functions (Allain et al., 2007; Raz, 2000; Shallice, 1982; West, 1996), which are a heterogeneous set
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of high-level cognitive processes that allow the subject to show flexible behavior and adapt to new
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situations(e.g., anticipation, planning, monitoring and control of action; problem solving; task flexibility;
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selection of relevant information; inhibition of automatic responses; and the exclusion of information that
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isirrelevant for the execution of a given task).All of these functions are involved in both encoding and retrieving
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information (Benton, 1994; Isingrini and Taconnat, 2008). Research in this area has repeatedly shown that
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alterations in the PFC negatively impact the functioning of memory, especially in its strategic aspects; EM
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deficits are also likely to reflect the degradation of certain cognitive resources, such as speed processing,
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inhibitory functions and attentional resources(e.g., Glisky, 2007; Groth and Allen, 2000; Wascher et al., 2012).
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The first data regarding cognitive aging, particularlychanges in EM, were collected from studies of
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brain-damaged patients (Wheeler et al., 1995; for review, see Werkle-Bergner et al., 2006)and experimentally
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lesioned animals (Aggleton and Brown, 1999; Miller and Cohen,2001). More recently, functional neuroimaging
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techniques, such as functional Magnetic Resonance Imaging (fMRI) and Positron Emission Tomography (PET),
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have been used to determine the brain modifications related to this decline. Meanwhile, cognitive aging studies
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have described the effects of aging on behavioral performance, and neurobiological studies have characterized
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the effects of aging on the brain. Then, in vivo neuroimaging techniques have been used to bridge the gap
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between these two techniques, allowing researchers to characterize the brain in action and examinethe neural
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substrates of cognitive aging that link behavior and function.The present paper aims to review neuroimaging
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results, especially fMRI and PET studies, andexplore the functional and cerebral activations associated with EM
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and behavioral disorders in the healthy elderly and patients with Alzheimer-type dementia.
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- Insert Figure 1 about here –
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2/ Episodic memory processes and cerebral substrates
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A major feature of the EM system, unlike other systems of LTM facing the present,is the ability to be
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aware of personal memories. This arises via“mental time travel” (Tulving, 2002), which is our ability to relieve
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past experiences and project ourselves into the future. EM is fundamental to the individual, as memories of
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personal experiences form the basis for the construction of identity. This memory can be tested verbally or non-
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verbally.During an episodic retrieval task,an individual is usually able to associate an EM (e.g. a word from a
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list) with particular details, such as the relevantemotion, time, place, and other particulars. The quality of
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memory storage depends on the processes involved in the encoding, storage and recovery of information (Figure
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2).
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2.1/ Encoding
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Encoding operates through the transformation of information that comes from external stimuli (e.g.,
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perceptual and sensory details, personal information, or spatial and temporal details) or triggers cognitive
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processes, and integrates the data in the form of a mental representation. Various sources are generally used to
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test experimental EM encoding; these can include verbal material (words), non-verbal material (pictures, scenes,
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objects, music, etc.), andthe context (i.e., source memory), the latter of which refers to the conditions
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surrounding the encoding of a particular episodic memory and the features under which it was acquired (Johnson
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et al., 1993). The context can serve as an indication for future recovery, asthe recollection of contextual details
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can allow an individual to distinguish a specific event from other similar events. During tests of contextual
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memoryparticipants are asked about the source of the experience (e.g.,Did person A or B report the event?), and
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various contextual details, including the color (e.g., Guo et al., 2013), vocal (e.g., Glisky et al., 2001), visual
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(e.g.,Fernandes and Manios, 2012), spatial (Cansino et al., 2015), and emotional (e.g., Bo and Xiao-Lan, 2012)
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context in which a word or event was presented. All of these details contribute to making EM multimodal,
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contextual, associative, and unique. Encoding is the first stage of memory, and it is crucial for the storage and
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retrieval ofvoluntary stored information. Many authors have described the processes of EM within a
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constructivist design (e.g., Schacter et al., 1998). During learning, the brain must form a neural representation of
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the new experience. A personally experienced episode is represented as a pattern of features that correspond to
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the different facets processed during the encoding of the episode(Gottlieb et al., 2012). These features are widely
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distributed in the brain, such that no single location contains a complete record of the memory trace of a specific
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episode(Squire, 1992). Multiple sensory structuresprocess the different stimuli and information regarding the
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identity of perceptualobjects and events. For example, the visual cortex is responsible for recognizing faces,
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letters, and the colors of letters, while the olfactory and auditory cortices recognize other facets of an experience.
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The neuronal activities arising from these cortices converge into the medial temporal lobe (MTL), where the
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perirhinal cortex, the lateral entorhinal area, the parahippocampal cortex and the medial entorhinal cortex treat
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the information.The inputs then converge at the hippocampus to become cohesive memories of individual events
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via the formation (“binding”)of EM (Kessels et al., 2007; Lekeu et al., 2002; Piolino et al., 2010). When such
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binding is faulty or absent, the individual may recover only fragments of the episode, not the whole pattern
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(Clayton et al., 2003). After binding, the outputs of the hippocampusreturn to the cortical areas from which the
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inputs arose (i.e., the perirhinal–lateral entorhinal cortex and parahippocampal–medial entorhinal
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cortex).However, information reaches the hippocampus every second of every day.The amygdala filters
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memories by evaluating their emotional content: if this latter is strong, this part of the brain informs the
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hippocampus to enhance storage of the event (e.g. Phelps, 2004).When an individual recalls a memory, the
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printed neural map in the hippocampus is reactivated, mobilizing the brain regions that were involved in forming
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the memory (i.e., the visual, olfactory and auditory cortices). This was shown by Wheeler et al. (2000), who
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reported that the sensory regions specifically activated during the encoding of images (occipital cortex) or
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sounds (temporal cortex) were reactivated when these memories were recalled. In parallel,a dialog between the
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hippocampus and the PFC allows the memory to re-emerge into consciousness (Preston and Eichenbaum, 2013).
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The type of information processing that occurs during the encoding stage determines the quality of both
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the encoding and the recovery of that information. Before the emergence of the neuroimaging techniques
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thatallow researchers to study the neuroanatomical bases of the encoding process, this process was primarily
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studied by manipulating the nature of the stimuli (verbal, pictorial), the sensory modality (auditory, visual), the
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time of presentation, and the way in which the studied individuals implemented strategies to better learn and
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remember information (e.g., mental rehearsal, phonological association, and organization of the material, such as
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through the construction of sentences or semantic categorization)(Gershberg and Shimamura, 1995; Turner et al.,
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2007).According to the treatment level design proposed by Craik and Lockhart in 1972, “the persistence of the
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memory trace is a function of the depth of treatment, levels of deep treatment being associated with more
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elaborate memory traces stronger in time, and more robust.”Indeed, the deeper the treatment, the stronger and
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lasting the memory trace. Superficial encoding simply relies on the structure of the stimulus (e.g. the number of
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vowels in a word), whereas deep encoding (e.g. the production of mental images) gives meaning to the stimulus,
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explores its relationship with other objects or situations, and thus has a positive impact on the memory trace(see
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Galli, 2014 for review).
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The relevant studies typically fall into two groups: intentional and incidental encoding studies. During
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the former, participants are scanned while attempting to memorize words, faces, objects, or spatial routes.
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During incidental encoding, in contrast, participants are usually asked to make a judgment concerning the stimuli
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presented during encoding (i.e., regarding semantics or size), without any attempt at memorization. To assess the
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neural bases of EM encoding using fMRI or evoked potentials, many authors have used the subsequent memory
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paradigm (also referred to as the “difference due to memory” or “Dm” paradigm) (Sanquist et al. 1980). In this
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paradigm, participants encode stimuli either intentionally or incidentally during scanning, and theneural activity
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associated with successful encoding of items that are subsequently remembered in a recognition test is compared
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to that observed during the encoding of items that are subsequently forgotten (Brewer et al., 1998; Wagner et
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al.,1998; for review, see Paller and Wagner, 2002). Several neuroimaging studies have shown, for example, that
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when neural activity supports successful encoding,thefMRI signal is greater for stimuli that are subsequently
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remembered compared to those that are forgotten (e.g. Bernard et al., 2004; Duverne et al., 2009; Kim, 2011).
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According to some studies, the encoding process seems to be disturbed by aging, with encoding
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deficiencies predominating over retrieval deficits in older adults (e.g. Friedman et al., 2007; Morcom et al.,
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2003). Nevertheless, encoding maintains a strong link with retrieval, and it is very difficult to separate the effects
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of encoding from those of retrieval in behavioral studies. This especially true given that retrieval tasks are used
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to measure memory performance,the success of retrieval depends on the success of encoding, andsome theories
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favor an overlap between these two processes.Most of the research on encoding has been conducted in rather
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young or rather old adults, with the younger adults usedas the reference group for comparison. This makes sense
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given that younger adults usually encode with much higher accuracy (Miller, 2013). Age-related declines in
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source memory are considered to be important for explaining the age-related deficits in EM. In
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addition,features(i.e. physical, visual, olfactory…) are less well remembered by older adults compared to
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younger adults, with older individuals showing poorer memory for the perceptual features of auditory inputs,
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such as a speaker’s voice (e.g. Bayen and Murnane, 1996).
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2.2/ Consolidation or storage
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After the encoding phase, a process of information consolidation is initiated, allowing performance to
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be maintained andreorganized into LTM.Two models of consolidation exist: the Standard Model (SM) of
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memory consolidation and the Multiple Memory Trace (MTT) (Nadel et al., 2007). First described by Scoville
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and Milner (1957), the SM theory stipulates that memory storage initially requires the hippocampus to linkthe
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different features of the memory, which are dispersed across numerous sites in the neocortex (Alvarez and
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Squire, 1994; Dudai, 2004; Squire and Alvarez, 1995). Over time, however, the requirement for the
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hippocampus dissipates (Meeter and Murre, 2004) and the representation of the memory becomes solely
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dependent on the neocortical storage sites (Frankland and Bontempi, 2005). This change in function over time is
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believed to account for the retrograde amnesia gradients often seen in patients with hippocampal damage. In
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contrast, the MTT theory posits that all memory traces incorporated since birth are combined into a multiple-
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trace representation in the brain. In this model, the hippocampus and neocortex continue to interact with each
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other during EM,forming the memory trace of an episode (Nadel and Moscovitch, 1997 for a review; Nadel et
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al., 2000). Contrary to the SM theory, the concept of MTTassumes that the MTL has no longer a temporary role
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in the storage and retrieval of memory but a permanent one. The hippocampus is always involved whenever
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detailed, contextual information is recalled (Hoscheidt et al., 2010; Piolino et al., 2008; Winocur et al., 2010;
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Figure 2). However, semantic information of the memory, which has no contextual richness and would then be
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more a schematic version of the memory, seems to be established in the neocortex alone(Harand et al.,
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2012;Nadel et Moscovitch, 1997).Episodic memories consolidation is measured by delayed recall in time of the
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previously recorded information (encoding) and after an interfering activity.However, this recall will only be
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useful if theimmediate free recall is correct (see below), insofar as only properly encoded information can be
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consolidated. Sleep is an important step in the consolidation of memory (e.g.Walker andStickgold, 2006), as the
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neural sequences involved in daytime learning are reactivated during the deep sleep and REM (Rapid Eye
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Movement)sleep phases (e.g. Rauchs et al., 2010). The effect of sleep on memory consolidation in aging has
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only been sparsely studied, and appears to be characterized by wide inter-subject variability in the elderly
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(Dudai, 2004; McGaugh, 2000; see also Alberini and Leroux, 2014).Therefore, we will only mention it briefly
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here.
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2.3/ Retrieval
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Unlike short-term memory, LTMrequires the retrieval of information that is no longer being maintained
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in an active state. Retrieval processes are required to reactivate its mental representations and return the
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individual to his or her conscious experience of the event (Tulving, 1983).The aging process strongly affects
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retrieval, but the importanceof such age-related differences may differ depending on the task used to assess EM
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performance (e.g., free recall, cued recall or recognition)(for reviews, see Balota et al., 2000; Brett et al., 2012;
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Craik and Jennings, 1992; Light, 1991; Luo and Craik, 2008; McDaniel et al., 2008; Zacks et al., 2000). In free
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recall (Arnold andMcDermott, 2013), a person is given a list of items to remember during encoding (e.g., words,
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sounds or pictures) and is then tested by being asked to recall as many items as possible in any order following a
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delay of variable duration. The experimenter notes the number of items correctly recalled as well as the number
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of intrusions (words that were not studied but are mistakenly recalled), which is more likely in AD patients than
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in normal controls (Dalla Barba and Wong, 1995).
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In cued recall, a person is given a list of items to remember during encoding and is then tested with cues
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aimed at helping them remember the material, such as the shape of the first two or three letters of an encoded
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word, or the first word of a pair ofencoded words.
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Recognitionrefers to an individual’s ability to judge whether an event or item had been
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previously“lived” or “seen”.Participants study a list of stimuli, and are then scanned while being given an old–
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new recognition test in which they are asked to judge whether they recognize the item as “old” (seen during the
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study phase) or “new” (Besson et al., 2013 for a review). Within the settings of either an event-related fMRI
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paradigm or event-related potentials, the neural activity associated with correct “old” responses (hits) is
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contrasted with the activity associated with correct “new” responses (correct rejections). Two other basic
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categories of recognition memory errors are often encountered during memory tests: false alarms (i.e., false
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recognitions) and misses(i.e., the failure to identify a previous occurrence as old) (Schacter et al., 1997). These
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memorydistortions (or false memories) occur when a remembered event either never occurred or the memory
342
differs substantially from reality.False memories can be experimentally induced by usingtheDeese-Roediger-
343
McDermott (DRM) paradigm, (Roediger and McDermott,1995).
344
In recent years, the measures of EMin recognition studies have evolved to take into account two
345
essential components: responses that depend on controlled retrieval (“recollection”) and those that rely on a
346
simple judgment of familiarity. Recollection is defined as “the mental reinstatement ofa previous event”
347
(Skinner and Fernandes, 2007). Details of a memory are recalled, such as the sounds associated with an event,
348
the emotions felt during the first presentation of the item or event, and/or the mental state of the subject being
349
tested. Familiarity, in turn, refers to the subject’s being able to sense that an event (or an item) has been
350
experienced in the past, but being unable to recall any detail. Thus, it is possible to achieve some memory tasks
351
when the recall is impaired and but the familiarity (or lack thereof) is not. The form of consciousness associated
352
with the memory also distinguishes these two forms of response, with autonoetic consciousness associated with
353
EM for recollection, andnoetic consciousness involving internal representations and linked to semantic memory
354
for familiarity(Gardiner and Richarson-Klavehn, 2000). Using the Remember/Know paradigm (R/K; Tulving,
355
1985), it is now classical to separately evaluate these two forms of information accessusing an introspective
356
approach that aims to assess the state of consciousness that accompanies recognition.For each item classified as
357
“old” on a recognition test, participants are asked to indicate whether their memory is vivid and rich in
358
contextual detail (“Remember”): whether the item was written in color, as well as whether upper- or lowercase
359
was used, whether they can describe the experimenter’s voice, whether the task was auditory,or whether the
360
participant classified it as “old” based on a non-specific sense of familiarity rather than a vivid memory
361
(“Know”) (Gardiner, 1988; Gardiner and Java, 1993; Yonelinas, 2002, see Migo et al., 2012 for a review). If the
362
participant seems to have trouble making a decision, he or she may be questioned regarding thedegree of
363
certainty (for review, see Gardiner et al., 2002). Another approach involves analyzing confidence judgments
364
with the Receiving Operator Characteristics (ROC) method (Yonelinas, 2001). During the recognition task,
365
participants must judge whether they have a high or low degree of confidence that theysawa given item during
366
the encoding task, or if they think the item was not previously presented.
367
In their review focusing on the brain networks underlying episodic memory retrieval, Rugg and Vilberg
368
(2013) stated that the recollection of information isassociated with the engagement of a neural network that is
369
centered on the MTL and includes the hippocampus, parahippocampus, and perirhinal cortices. Together, they
370
are interconnected with cortical regions (e.g., theretrosplenial and posterior cingulate cortex, the angular gyrus,
371
and the medial and lateral prefrontal cortex; mPFC)to retrieve past events(Figure 2).
372 373 374
-Insert Figure 2 about here -
375 376
11
377
3/ Behavioral data and models clarifying the memory decline performance in normal aging
378
EM performance gradually deteriorates from middle age through young-old age to old-old age (Nyberg
379
et al., 2003).With aging, many aspects of information processing become less efficient, and both episodic
380
encoding and retrieval processes are impaired (e.g. Anderson et al., 2005; Giffard et al., 2001;Gutchess et al.,
381
2007; Morcom, 2003). Older individuals suffer from difficulties in retrievingthe encoding context and stored
382
information in a rich and detailed way; exhibit increases in the number of false recognitions; show decreases in
383
inhibition capacities that may be explained by problems with the self-initiated development of encoding
384
strategies(e.g., Bastin and Van der Linden, 2005; Fernandes and Manios, 2012).
385
The quality of the sensory information presented to the cognitive system (Craik and Rose, 2012) and the
386
duration it remains available for processing (Walsh and Thompson, 1978) can affect the encoding of memory in
387
older adults. EM is traditionally assessed using verbal memory tasks. The age-relateddecline in itsencoding was
388
supported by Park et al. (1989), who asked young and older adults to categorize words while performing a
389
number-monitoring task during encoding, retrieval or both. The authors found that the performances of older
390
adults were more highly impaired when their attention was divided during episodic encoding,whereas their
391
performance on retrieval tasks was similar to that of the young participants.Moreover, an insufficiently precise
392
and distinctive encoding can lead to false recognitions (e.g. Dennis et al., 2007b; Murphy et al., 2007; Rosa and
393
Gutchess, 2013), which arise mainly when new items presented during retrieval are closely related to those
394
encountered during encoding (e.g. Kensinger and Schacter, 1999; Koutstaal and Schacter, 1997).Recognition
395
tests that include semantic distractors (e.g. “dahlia” or “petunia” for the flowers category) yield more false
396
recognitions in the elderly than among young subjects. This suggests that general-level encoding allows the
397
elderly to reject semantically unrelated distractors (e.g. “camel”), whereas the correct discrimination of
398
semantically related items requires more elaborate encoding. In their meta-analysis, Spencer and Raz (1995)
399
reported that age had a differential effect on recall performances depending on the type of encoding (incidental
400
or intentional). Taconnat and Isingrini (2004) manipulated the conditions of encoding using the production
401
paradigm, which holds that memory is substantially benefited byproducing/generating the second word of a
402
word pair as opposed to just reading it. Young subjects were found tobenefit from both semantic and
403
phonological cues, while older subjects benefited from the production of the item only when there was a
404
semantic relationship between the item and the clue. This suggests that memory in the elderlycan benefit from
405
deep or semantic processing at encoding, but only when the conditions of encoding strongly guide the desired
406
operations. Finally, age-related deficits during encoding may also depend on the utilized stimuli. For example,
407
scene encoding tends to differ little with age because, unlike the recognition of words, that of non-verbal
408
material(e.g. pictures) is largely age-invariant (e.g.,Craik and Jennings, 1992; Gutchess et al., 2005; Park et al.,
409
1986).Individuals tend to better remember rich and meaningful stimuli (such as pictures) because such stimuli
410
automatically engage multiple representations and associations with other information about the world, leading
411
to more elaborate encodings (e.g., Craik and Rose, 2012).One possible explanation for the effects of normal
412
aging on EM results is the acquisition of a deficit in the strategic processes involved in encoding (Shing et al.,
413
2010). Indeed, the lower performance of the elderly on memory tests has been attributed to a lack of self-
414
initiated processes (Craik, 1990; Kausler, 1994; Sauzéon et al., 2000), whichleads to difficulties in implementing
415
the spontaneous cognitive operations required for optimal memory (Craik, 1986). Indeed, when verbal encoding
416
is incident or superficial,or where no task is requested, the elderly spontaneously engage in less effective
417
strategies. The task does not directly guide the subjects in establishing an encoding strategy; they must initiate it
12
418
by themselves, and their chosen strategy typically does not increase their memory performance (Guillaume,
419
2009; Taconnat and Isingrini, 2004; Van der Veen et al., 2006). For instance, Dunlosky and Hertzog (2001)
420
found that when subjects were given the freedom to choose a strategy from among four possibilities in order to
421
encode pairs of words, young subjects used more mental imagery and sub-vocal rehearsal strategies, whereas
422
older subjects tended to generate sentences with the two words or use no strategy at all. The authors proposed
423
thatthe performance decreases of middle ageseem to reflect a failure to initiate elaborate procedures rather than a
424
deficit in the encoding processes per se. After 60 years of age, encoding becomes less effective even in the
425
presence of aids and clues, and the mechanisms for developing and allocating attention are insufficient.When
426
environmental support is high, however, such individuals can process the information deeply. For example,
427
when old adults make a mental image, use a word in a sentence, or give a synonym during the encoding of a
428
word (Craik and Jennings, 1992), the memory trace is strong and durable; thisyields better test performance and
429
less performance difference between young and elderly participants (e.g.,Dunlosky et al., 2005; Froger et al.,
430
2009; Kalpouzos et al., 2009; Logan et al., 2002; Taconnat et al., 2008) regardless of the time spent studying the
431
items. In other words, a deep and semantic encoding, even performed over a relatively shortperiod, is more
432
effective than a superficial treatment made over a longer period (Craik and Tulving, 1975). The two factors of
433
“self-initiated processing” and “environmental support” are complementary, with less environmental support
434
meaning that more self-initiated processing must be deployed and vice versa.
435
Age-related memory deficits are also present during retrieval, and elderly people routinely forget things.
436
The interference theory (Dewar et al., 2007) suggests that such forgetfulnessreflects the similarities between
437
memorized materials, in that memory can be disrupted by what we have previously learned (old memories
438
interfere with the retention of new learning) or by what we will learn in the future (new learning interferes with
439
the retention of old memories). For example, it can be difficult to remember how to use an old phone when
440
learning to use a new one; this is an example of a competitive response leading to lower memory performance
441
(Blank, 2005; see also Fandakova et al., 2013).In the elderly, the degreeof the memory deficit varies depending
442
on the task:age-related differences are more pronounced in free recall tasks that require the subject to
443
spontaneously retrieve a previous episode without any external help, compared to cued recall or recognition
444
tasks, in which an index is provided to facilitate the mental research of the stimulus. The performances of older
445
subjects are inferior to those of young subjects during free recall, whereas the age groups are often equivalent
446
intheir recognition abilities(Craik and McDowd, 1987; Isingrini et al., 1996; Sauzéon et al., 2014; Taconnat et
447
al., 2009). These patterns of performance could be explained by insufficient encoding, in that the memory trace
448
is too weak to be reactivated during free recall but is sufficient for recognition. Old people have more difficulties
449
in spontaneously generating cues to retrieve information in memory (Dunlosky et al., 2005; Sauzéon et al.,
450
2001;), but they exhibit normal benefits from receiving semantic cues during such retrieval (e.g., Monti et al.,
451
1996).Work using the R/Kparadigm (Guillaume, 2009; Rajaram, 1993; Richardson-Klavehn et al., 1996) has
452
indicated that the elderly can have difficulty accessing the contextof learning (Bugaiska et al., 2007; Clarys et
453
al., 2002; Jacoby, 1991; Jennings and Jacoby, 1997; Prull et al., 2006). The ability to control the source of
454
information decreases with age, making subjects particularly vulnerable to false memories (Dodson and
455
Schacter, 2002; Johnson et al., 1993; Lövden, 2003). For example, Jacoby and Rhodes (2006) found that the
456
elderly were more likely to accept false information as true, compared to young adults. In addition, older
457
individuals had a greater sense of confidence in their misjudgmentscompared to young subjects (Dodson et al.,
458
2007). The proportion of Remember responses (R), which reflect the recovery of every contextual detail,
459
declines with aging, whereas the proportion of Know responses (K), which are associated with a sense of
13
460
familiarity, remains stable or increases slightly (e.g. Clarys et al., 2009).Older adults would therefore tend to
461
develop recovery processes based primarily on familiarity,but might struggle to identify the source of this
462
familiarity using contextual elements. In other words, age affects the quality and richness of the information
463
retrieved from memory. Fewer details are recalled and episodes are relived less frequently. This notion has been
464
reinforced by the observation of lower performance in the elderly on memory source tasks, compared to younger
465
subjects (Mitchell et al., 2003; Spencer and Raz, 1994).
466
In addition to strategic deficits, attention and processing speed may be critical components of the age-
467
related decline in EM function (see Park and McDonough, 2013). Craik (1986) hypothesized that the amount of
468
attentional resources available to initiate and carry out cognitive processes could decrease with age (Craik and
469
Jenning, 1992). The attentional demands of both encoding and retrieval are greater for older adults than for
470
young adults, although this age difference is most pronounced for retrieval (Craik and McDowd, 1987; Whiting
471
and Smith, 1997). Older subjects are less able to spontaneously develop the most effective encoding and retrieval
472
operations, because such operations are very expensive in terms of attention (Anderson et al., 1998). However,
473
other studies showed that the presence of a sufficiently large environmental context at the time of encoding (e.g.,
474
a semantic task) and/or retrieval (e.g., a clue) could minimize the need for a costly self-initiated treatment in
475
attention and reduce the memory impairment associated with age (Craik, 1986; Craik and Byrd, 1982).
476
The theory of cognitive slowdown proposes that changes in the processing speed significantly
477
contribute to age-related cognitive performance declines, leading to less effective encoding and increasing the
478
time required to retrieve stored information (Bunce and Macready, 2005; Clarys et al., 2002; Hertzog et al.,2003;
479
Perrotin et al., 2006; Salthouse, 1996).Indeed, when comparing elderly and young groups in recognition-based
480
retrieval, Daselaar et al. (2003) showed increased reaction times in the latter group, indicating that there is likely
481
to be an age-related slowing of motor responses. This model is based on the consistent observation that
482
processing speed shows a linear decrease during early adulthood, and that this decrease may accelerate in late
483
old age (Feyereisen & Van der Linden, 1997; Salthouse, 1993a, 1993b). Two distinct mechanisms appear to be
484
responsible for the relationship between processing speed and cognition:1) cognitive operations are performed
485
too slowly to be achieved in a limited time, and less cognitive processing is generally associated with a lower
486
level of performance; and 2) the slowdown reduces the amount of available information, which isneeded for the
487
execution of higher-level cognition.In the elderly, this slowdown primarily affects the encoding operations,
488
resulting in the creation of fragile memory representations.
489
It has also been established that normal aging is accompanied by a decrease in an individual’s capacity
490
to inhibit the acquisition of irrelevant information on the verbal, motor, attentionalandmnesic levels (Connely et
491
al., 1991; Potter and Grealy, 2006; Spieler et al., 1996).The inhibitory capacity can be defined as the set of
492
sequential processesimplemented to prevent the emergence of an automatic or context-induced response, or
493
(conversely) to prevent irrelevant information from entering theattentional field. However, the performance of
494
the elderly can reportedly becomparable to that observed in young subjects,indicating that not all aspects of
495
inhibitory function undergo age-related alterations. For example,Jennings and Jacoby (1993) demonstrated that
496
some age-related memory differences are due to declines in controlled (but not automatic) information
497
processing for verbal (Healy et al., 2005) or non-verbal (Zelazo et al., 2004)materials (see also Hasher and
498
Zacks, 1979;Jacoby et al., 2001; Yonelinas, 2002). Indeed, the concept of controlled retrieval implies that there
499
is an intentional effort to initiate research in memory and consciously control and mobilize attention throughout
500
the task, all of which are costly processes.
14
501
In
sum,
normal
aging
is
usually
accompanied
by
declines
in
various
behavioral
502
performanceseitherduring encoding or retrieval or even during both phases according to the stimuli, the
503
paradigm, the environment and the strategies used by the person.Nevertheless, a change in the organization of
504
the neural networks underlying EM can also be responsible for the difference seen between young and older
505
adults.
506
4/ Chemical and anatomical data: role of brain imaging study in healthy elderly
507
The age-related decline in EM seems to reflect the depletion of neurotransmitters as well as age-related
508
degradation of the brain’s anatomy and physiology (Coleman and Flood, 1987; for review, see Grady, 2012).
509
Recently, the advent of non-invasive neuroimaging methods (e.g., fMRI and PET) has enabled researchers to
510
examine normal memory processes in the healthy brain (Spaniol, 2009), yielding a better understanding of the
511
links between cognitive skills and neural substrates. The earliest cognitive and neuroanatomical information
512
about EM originated from the study of patients suffering from amnesic syndrome or frontal lesions (Squire,
513
1992). Indeed, if these patients do not have real amnesic syndromes, they experience similar difficulties than
514
older subjects. Older adults, as brain-frontal subjects, exhibit more intense deficits in memory tasks that require a
515
significant contribution by controlled processes, such as free recall.
516
Investigations using non-human primates and neuropsychological approaches have revealed activation
517
patterns that indicate the existence of a relatively wide neuronal network underlying EM (Andreasen et al., 1995;
518
Cabeza et al.,1997; Cabeza and Nyberg, 2000; Desgranges et al., 1998; Nyberg et al., 1996a; Nyberg et al.,
519
1996b; Rugg and Vilberg, 2013; Shimamura, 2014). It mostly comprises the PFC, the MTL and particularly the
520
hippocampus but also the parietal cortex.Neurofunctional changes in these regions also seem to be correlated
521
with age-related memory declines and learning difficulties (Head et al., 2009; Raz, 2000; Raz et al., 2005;
522
Yonelinas et al., 2007). For example, Rajah and colleagues (2011) found that age-related reductions in the
523
volume of the medial frontal gyrus were negatively correlated with retrieval activity in the same regions during
524
an EM task.
525
4.1/ Depletion of neurotransmitters
526
With respect to disorders of neurotransmission associated with cerebral aging, converging arguments
527
indicate that dopamine deficiency is the main neurobiological determinant of the aging brain. DA function has
528
traditionally been linked to motor performance (Freed and Yamamoto, 1985) and reward-related processes
529
(Baudonnat et al., 2013; Schultz, 2006; Wise, 2004). Authors demonstrated that DA is truly a learning signal
530
(Schultz, 1998) and is invoved in learning of a stimulus-reward association (Waelti et al., 2001). This
531
neurotransmitter codes for incentive salience, the neural process that generates the desire and motivates an
532
individual to act in order to get the reward (Berridge and Robinson, 1998). For example, mice deprived of DA
533
are still sensitive to rewards but fail to motivate their behavior. In monkeys, DA amplitude discharges better
534
correlate with the level of motivation than with the size of the reward (Satoh et al., 2003).More recently, DA has
535
been associated with higher cognitive abilities, such as attention and memory processes (Starter and Bruno,
536
2004), in patient populations with severe damage to the DA system, such as those afflicted with Parkinson
537
Disease and Huntington Disease (Brown and Marsden, 1988), as well as in lesion studies in monkeys (Goldman-
538
Rakic, 1998), and pharmacological studies using DA agonists in younger volunteers (Luciana et al., 1998).
15
539
Functional neuroimaging studies have demonstrated that interaction between reward-related regions
540
(orbitofrontal, ventral tegmental areas, striatum, PFC or substantia nigra) and memory-related regions including
541
the MTL structures, could contribute to the memory enhancement by reward motivation (e.g., Tsukiura and
542
Cabeza, 2008; Wittmann et al., 2011; Wolosin et al., 2012). Some studies have shown that reward improves
543
memory formation in incidental and intentional encoding paradigms (Wittmann et al. 2005; Adcock et al. 2006;
544
Callan and Schweighofer 2008; Wittmann et al. 2008). Others demonstrated that higher-value (i.e. high
545
monetary reward) items are remembered better than low-value items (i.e. low monetary reward) (e.g. Adcock et
546
al., 2006; Wittmann et al., 2005; Shigemune et al., 2010). Nevertheless, Madan and Specth (2012) recently
547
reported that memory is enhanced not only due to reward value but also to reward salience (highest and lowest
548
value items are remembered best and intermediate-value items are remembered worst). Reward has also been
549
demonstrated to abolish the so-called « Retieval-Induced Forgetting » (Imai et al., 2014), a memory phneomenon
550
where remembering causes forgetting of other information in memory. It is believed to prevents us from
551
becoming confused between information we’ve made an effort to learn and closely related information we didn’t
552
strive to learn. Reward overall enhanced memorized items and abolished the suppression of the retrieval of non-
553
learned items. However, a depletion of DA can have a consequence on the « reward –effect ». Lesion of some
554
dopaminergic pathways (e.g. nigrostriatal pathway), as well as pharmacological blockade of DA receptors,
555
makes the animals insensitive to rewarding effects, result in a lack of interest for environmental stimuli and a
556
decrease in exploratory behavior (Di Chiara, 2002; Wise, 2008). The duration of reward was reduced by
557
dopaminergic antagonists (Yokel and Wise, 1975; 1976). DA depletion has also been linked with reward theory
558
in healthy aging. Indeed, Dreher and colleagues (2008) demonstrated that the coupling of midbain DA synthesis
559
and reward-related PFC activity was altered in older adults. DA reward reponse appears to code the discrepency
560
between the reward and its prediction. This « prediction-error » seems to be altered in older adult, resulting in an
561
abnormal signature of expected value and then an incomplete reward prediction error signal. Chowdhurry and
562
her colleagues (2013) found that this abnormal reward procesing in aging can be restores with DA (see also
563
Eppinger et al., 2011). Healthy aging has also been show to induce functional altertions in the reward system
564
Wong et al. (1997) found a decrease in the number of dopaminergic receptors with age. In vivo studies
565
using PET found smaller (but reliable) age-related declines in the human striatum, responsible for a large
566
proportion of DA production. This area has extensive connections to the PFC (Graybiel, 2000)and might
567
therefore affect the cognitive processes that are sub-served by DA-dependent circuits (Hedden and Gabrieli,
568
2004). Post-mortem evidence indicates that age induces substantial losses in both pre- and postsynaptic markers
569
of the DA system (Fearnly and Lees, 1991). Likewise, PET findings demonstrate marked age-related decreases
570
in DA function for presynaptic markers, such as L-DOPA utilization and DA transporter density (VanDyck et
571
al., 1995; Volkow et al. 1996) as well as for postsynaptic markers, such as D1 and D2 receptor binding. Age-
572
related decreases in performance were significantly correlated with D2 receptor availability and binding
573
(Bäckman et al., 2000; Erixon-Lindroth et al., 2005). Furthermore, intermittent stimulation of dopamine D1
574
receptor systems was shown to improve delayed response performance for older monkeys while having a small
575
detrimental effect for young monkeys. These beneficial effects remained in effect at 1 year following
576
stimulation. Dopamine stimulation might thus specifically benefit populations with deficiencies (older adults)
577
and could provide the basis for treating even normal age-related declines (Castner and Goldman-Rakic, 2004). In
578
a pharmacological fMRI study, Morcom et al. (2010) showed that elderly subjects with worse recognition
579
performance scores on EM tasks were more sensitive to dopaminergic modulation induced by bromocriptine (a
580
D2-like receptor agonist) or sulpiride (a D2-like receptor antagonist), as reflected by activity in the left MTL
16
581
during efficient EM encoding. Age-related losses of DA have also been observed in non-striatal structures,
582
including the frontal, temporal and occipital cortices, as well as the hippocampus and thalamus (Inoue et al.,
583
2001; Kaasinen et al., 2000).
584
Acetylcholine is another neurotransmitter that plays an important role in memory (Deutsch, 1971; Gold,
585
2003; Hasselmo, 1999; 2006). The two main subtypes of cholinergic receptors, nicotinic and muscarinic, are
586
both sensitive to the effects of age (Giacobini, 1990; Nordberg et al., 1992), and cholinergic deficiency has been
587
suggested to explain at least part of the age-related declines in memory performance (Gallagher and Colombo,
588
1995; Taylor and Griffith, 1993). Memory performance decreases comparable to those observed in elderly
589
subjects were demonstrated in young subjects after scopolamine-induced blockade of muscarinic receptors
590
(Jones et al., 1991), but it is not yet known whether a cholinergic deficit can affect memory directly, or indirectly
591
alter it by disturbing attention (Blokland, 1995; Everitt and Robbins, 1997; Hasselmo and Bower, 1993; Voytko,
592
1996). In a resting-state fMRI study, Wink et al. (2006) found that the administration of scopolamine to young
593
healthy subjects mimicked the dynamics of hippocampal activity observed in placebo-treated elderly subjects,
594
suggesting that a cholinergic mechanism may underlie the age-related changes in EM.
595
4.2/ Prefrontal cortex
596
The results from brain imaging and behavioral studies on age-related morphological brain changes
597
converge to suggest the presence of critical alterations in the PFC brain region, which is associated with
598
executive functions (West, 1996; Kalpouzos et al., 2009). This supports the frontal hypothesis, which holds that
599
executive functions are the first cognitive functions to decline during aging, leading to the strongest and earliest
600
age-related changes in the cognitive skills that depend on such functions (Taconnat et al., 2007). With respect to
601
memory, declines in executive function impair strategic, controlled processing at the levels of encoding and
602
retrieval. Memory profiling of frontal brain-damaged patients and neuroimaging studies have shown that there is
603
a close link between memory (especially EM) and frontal activity (Cabeza, 2002). The frontal lobes play key
604
roles in acquiring and encoding information, retrieving information in the absence of contextual cues, recalling
605
the source of information, and assessing the temporal sequence and recency of events. Relevant functional
606
dissociations have been found within the frontal cortex (e.g.,Blumenfeld and Ranganath, 2006, 2007; Rypma and
607
D’Esposito, 2003); the ventrolateral region contributes to selecting appropriate information, while the
608
dorsolateral area organizes the information in working memory. These two regions thus play complementary
609
roles leading to the formation of EM.
610
4.3/ From HERA to HAROLD: the compensation models
611
Kapur et al. (1994) used PET to study EM in 12 healthy volunteers and observed important activations
612
of the left inferior PFC (Brodmann areas 45, 46, 47 and 10) during an encoding task and the right dorsolateral
613
frontal cortex (Brodmann areas 10, 46, 9) during a recall task. This asymmetry led scientists to propose the
614
HERA (Hemispheric Encoding/Retrieval Asymmetry) model (Tulving, 1994), which holds that the left frontal
615
cortex is preferentially involved in episodic encoding, whereas the right frontal cortex is preferentially involved
616
in episodic retrieval. Others studies also found unilateral activity in young adults (e.g., Cabeza et al., 2004; Davis
617
et al., 2012; de Chastelaine et al., 2011; Reuter-Lorenz et al., 2000; Schneider-Garces et al., 2010; for reviews,
618
see Cabeza and Nyberg, 2000; Fletcher and Henson, 2001). Regions in the left PFC are consistently activated
17
619
during the encoding of non-verbal material (e.g., object localization, Ownen et al., 1996; unknown faces, Grady
620
et al., 1995). Conversely, right PFC activation is seen during the retrieval of episodic information (Morcom et
621
al., 2003), as extensively demonstrated with paradigms using free recall, cued recall, or recognition of diverse
622
stimuli, such as sentences, drawings of objects, words, faces, smells, melodies, and colored geometric patterns
623
(e.g., Nyberg et al., 1996; Bernard et al., 2001; Platel et al., 2003). Notably, however, some authors have failed
624
to confirm these results and found bilateral recruitment of the PFC (e.g., Kelley et al., 1998; Spaniol, 2009). It
625
was suggestedthat the PFC is bilaterally recruited when a task requires increased cognitive resources (Cairo et
626
al., 2004; Nolde et al., 1998), thereby showing a pattern similar to that observed in older adults during the
627
performance of simpler tasks. In 1998, Nyberg proposed that parts of the right PFC should be distinguished into
628
the right anterior PFC, which is involved in all memory tasks, and the right posterior PFC, which is involved in
629
the more difficult retrieval operations. Together, these findings suggest that the HERA model is modulated by
630
the nature of the material (Fliessbach et al., 2006; Golby et al., 2001; McDermott et al., 1999; Wagner et al.,
631
1998), the complexity of the task (Nolde et al., 1998) and the involved memory process (e.g., Iidaka et al., 2000;
632
Nyberg et al., 2000).
633
Given the imaging studies showing the consistent involvement of PFC regions in memory among
634
younger adults and their central role in cognitive aging, it is of critical interest to study PFC activity in the
635
elderly. The structural and behavioral data discussed above suggest that one might expect neural activity to
636
decline with age (e.g., Logan et al., 2002; for review, see Park and Gutchess, 2004), consistent with the declines
637
in cognitive function and brain structure. Quite surprisingly, numerous neuroimaging studies of EM have shown
638
that the functional brain activity in the PFC increases with age across a range of tasks, with increases in right
639
frontal areas and reductions in left frontal activity during encoding(e.g., Anderson et al., 2000; Cabeza, 1997;
640
Grady et al., 1995; 2002; Leshikar et al., 2010; Morcom, 2003; Nyberg, 1996a, 1996b; Rosen et al., 2002; for
641
review, see Dennis & Cabeza, 2008) and vice versa during EM retrieval. This bilateral pattern of PFC activity in
642
the elderly reduces their hemispheric asymmetry, as reflected in the HAROLD model (Hemispheric Asymmetry
643
Reduction in OLDer Adults) proposed by Cabeza (2002). Additional prefrontal recruitment is tought to be a
644
general characteristic of age-related neural change (Cabeza et al., 2004; Davis et al., 2008; for review, see
645
Spreng et al., 2010). This lack of asymmetry is observed in a wide range of tasks, including word recall after
646
incidental learning (Logan et al., 2002; Stebbins et al., 2002), intentional learning (Logan et al., 2002), delayed
647
recall (Morcom et al. 2003), and memory retrieval (Bäckman et al., 1997; Hatta et al., 2015). But in the field of
648
pictorial stimuli in young subjects, older adults cannot engage bilateral regions as predicted by the HAROLD
649
model as both hemispheres are already activated in young adults (Golby et al., 2001; Kelley et al., 1998).
650
Gutchess et al. (2005) hypothesized that older adults would show increased prefrontal activations in regions not
651
activated by young adults. While both young and older adults showed bilateral activations of the inferior frontal
652
gyri during the successful encoding of pictures of outdoor scenes, the older adults showed more activation of
653
several other frontal regions (including the left middle frontal gyrus) compared to younger subjects.
654
Two interpretations have been proposed to account for the HAROLD phenomenon in aging. In the
655
absence of memory decline in elderly people, a more widespread activation pattern is interpreted as reflecting
656
either: 1) difficulty in engaging specialized neural mechanisms, which is a phenomenon called
657
“dedifferentiation” (e.g., Li and Lindenberger, 1999; Logan et al., 2002); and/or 2) an optimized cognitive
658
mechanism (i.e., the use of a cognitive strategy different from that of younger adults) to deal with the executivo-
659
frontal dysfunction that accompanies normal aging (Reuter-Lorenz and Lustig, 2005; Stern et al., 2009; for
660
review, see Cabeza, 2004). The latter compensation phenomenon suggests that older individuals engage both
18
661
hemispheres in some tasks that require only one hemisphere in young subjects; this compensates for cognitive
662
deficits, and is thus positively correlated with successful cognitive performance (Reuter-Lorenz et al., 2000; Park
663
et al., 2003). Concerning encoding, the age-related shift from left lateralized processing to a more distributed
664
pattern corresponds not only to encoding attempt, but mostly ultimate success. Indeed, activating a second
665
hemisphere would increase the resources that the elderly have available (Ska, 2006) to generate the same
666
functional result as their younger peers (Cabeza et al., 2002, 2004). This additional frontal recruitment allows
667
older adults to maintain a good level of accuracy at the expense of a slower reaction time (Grady et al., 1994; but
668
also see Reuter-Lorenz et al., 2000). Some studies have suggested that age-related over-recruitment is observed
669
in only a few PFC regions, such as the bilateral medial and superior frontal gyri (Gutchess et al., 2005), and in
670
the bilateral anterior superior frontal gyri (Morcom et al., 2003). In contrast, bilateral activation of the PFC in
671
older adults is not always related to better performance. In a recent review (2012), Grady reported that some
672
authors found greater recruitment in the PFC during memory encoding (de Chastelaine et al., 2011) and retrieval
673
(Persson et al., 2011) in elderly participants, but this was correlated with poorer memory. Similar results were
674
obtained during word recognition (Madden et al., 1999), facial recognition (Grady et al., 2002), and spatial tasks
675
(Piefke et al. 2012; Meulenbroek et al., 2010).
676
In a PET study, Bernard et al. (2007) tested young and elderly subjects in a cued recall task. The
677
activation of the right PFC was similar in the two groups, but there was a significant between-group difference at
678
a behavioral level, with the older subjects showing lower-level performance. This apparent paradox was solved
679
by taking into account the results of a previous study in which two groups of older subjects were scanned while
680
performing episodic retrieval of verbal material: a group of “low-performers” with significantly lower episodic
681
retrieval performances compared to young healthy subjects; and a group of “high-performers” with
682
performances comparable to those of young subjects (Cabeza et al., 2002). Similar to the young participants, the
683
low performers showed activation of only the right PFC. In contrast, the elderly high-performers showed
684
activation of both the right and left PFC, suggesting that their brains were working harder and engaging in a
685
more distributed compensatory process. According to Park (2009), the additional activation of the contralateral
686
hemisphere reflects the inefficient operation of inhibitory mechanisms. Overall, these results suggest that there is
687
a three-way interaction among age, task difficulty, and fontal laterality.
688
A variety of theoretical models have been proposed to explain age-related over-recruitment (e.g.,
689
Cabeza and Dennis, 2013; Davis et al., 2008; Maillet and Rajah, 2013). The age-related decreases in brain
690
structure size and white matter integrity concomitant with increases in prefrontal activation prompted the
691
development of the Scaffolding Theory of Aging and Cognition (STAC; Park and Reuter-Lorenz, 2009), which
692
describes the brain’s response to cognitive challenge. This model posits that despite neural challenges and age-
693
related worsening, behavior is maintained at a relatively high level by the recruitment of additional circuitry.
694
With age, this compensatory scaffolding process may be invoked to perform familiar tasks and basic cognitive
695
operations, which become increasingly challenging as the existing neural circuitry degrades. In addition, the
696
over-recruitment of the PFC may reflect an attempt to compensate for age-related declines in other brain regions
697
(Cabeza et al., 2004; Gutchess et al., 2005; Goh et al., 2010). For example, the PASA model (Posterior-Anterior
698
Shift in Aging) (for review, see Davis et al., 2008) suggests that a decrease in posterior cortical activations (i.e.,
699
that of the occipito-temporal cortex) in older adults is accompanied by an increase in anterior activity,
700
particularly frontal. Some recent work suggests that PASA patterns may be particularly prevalent under more
701
taxing cognitive demands (Ansado et al., 2012), but the recruitment of additional brain regions might come with
702
a cost (Bäckman & Dixon, 1992; Cabeza, 2002; Reuter-Lorenz et al., 2008). For example, the recruitment of
19
703
contralateral hemispheres may reduce the brain’s ability to perform simultaneous tasks. Given that older brains
704
engage more neural circuitry at lower levels of task demand compared to younger brains, seniors rely more
705
heavily on their CR and are more likely to reach a limit on the resources that can be brought to bear on task
706
performance. Reuter-Lorenz and Cappell (2008) referred to this as CRUNCH (Compensation-Related Utilization
707
of Neural Circuits Hypothesis).
708
In applying the PFC function theory to cognitive aging, the work of West (1996) supported the
709
hypothesis that cognitive processes supported by the PFC are among the first to decline with increasing age.
710
However, differences were also observed on tasks that are traditionally considered to be “non-frontal” (e.g., item
711
recall and recognition), leading West to conclude that: “this age related decline in item recall and recognition
712
suggests that the frontal lobe hypothesis of aging provides a useful but incomplete neuropsychological model of
713
cognitive aging.” Some investigators have pointed out that the performance of memory tasks involves the
714
coordination of multiple neural systems beyond the prefrontal cortex. Indeed, the frontal hypothesis (which is
715
admittedly somewhat simplistic) should not obscure the roles of other brain structures (e.g., the parietal cortex),
716
especially when the real memory difficulties among older subjects could be better explained by MTL
717
dysfunction.
718
4.4/ Aging in the PFC: link with behavioral data
719
The HAROLDfinding was more prevalent in intentional versus incidental encoding studies, suggesting
720
that the environmental support provided by a deep encoding task may attenuate the age-related decreases in left
721
PFC activity (Daselaar et al., 2003; Dennis and Cabeza, 2008; Kapur et al., 1996; Logan et al., 2002; Morcom et
722
al., 2003). Nevertheless, a PET study by Bernard et al. (2001) showed that the intentional encoding of words
723
bilaterally activated the PFC, with a larger activation noted in the left hemisphere. Similarly, deep processing of
724
pictures triggered increased activity in the left PFC and bilateral medial temporal regions (Grady et al., 1999).
725
Deeper processing (e.g., semantic judgment tasks) was also shown to activate the inferior PFC and left
726
dorsolateral PFC (DLPFC) more strongly than a more shallow treatment (Demb et al., 1995; Fujii et al., 2002;
727
Iidaka et al., 2000; Otten et al., 2001; for review, see Galli, 2014). In an associative encoding task, older adults
728
showed a typical pattern of increased activity in the right inferior frontal region, the left inferior frontal gyrus,
729
and the left hippocampus as the task difficulty increased (Leshikar et al., 2010). Furthermore, activity in these
730
regions has been found to predict subsequent memory performance (Wagner et al., 1998; for review, see Park et
731
al., 2013). In young adults, activity in the PFC was found to predict the formation of successful memory (Brewer
732
et al., 1998; Kirchhoff et al., 2000), while a subsequent memory task showed that increased frontal activation in
733
older adults was associated with remembered items, but not with forgotten items (Gutchess et al., 2005).
734
Mitchell et al. (2004) also observed that young adults showed activation in the left
735
judgments, whereas older adults did not. The authors posited that the source memory deficits seen in older adults
736
might be related (at least in part) to reductions in the function of the left PFC region that is engaged by young
737
adults. Thus, the left PFC appears to be specifically involved in more complex memory tasks or those that
738
require encoding strategies (Fletcher and Henson, 2001). Patients with left frontal lesions present specific
739
deficits when the task requires semantic strategies during encoding (e.g., Incisa della Rocchetta and Milner,
740
1993), whereas their performances returned to normal when they were provided with semantic clues or
741
instructions on the use of specific strategies (Gershberg and Shimamura, 1995). Thus, one important function of
742
the PFC in memory is to focus behavior towards the development of a strategy aimed at optimizing memory
DL
PFC during source
20
743
performance. Specifically, the encoding-related activity in the ventrolateral PFC (VLPFC) is believed to reflect
744
the selection, maintenance, and control of incoming information (Blumenfeld et al., 2011), whereas activity in
745
the
746
Ranganath, 2007; Daselaar et al., 2006; Paller and Wagner, 2002; Simons and Spiers, 2003). Other studies have
747
emphasized the content-specific aspects of prefrontal function, with left-lateralized ventrolateral activity
748
appearing to be associated with verbal material and right-lateralized activity with visual material (Wagner et al.,
749
1998).
DL
PFC is thought to support organization and associative encoding (for reviews, see Blumenfeld and
750
Lepage et al. (2000) identified a set of regions associated with the “retrieval mode” (REMO) in EM.
751
The activation of the REMO sites is described as governing the subject’s neurocognitive state when the attention
752
is focused on a segment of the past; this state takes into account the relevant indices, inhibits the irrelevant
753
indices and supports effective access to the memory trace. The REMO sites include the anterior cingulate cortex
754
and various frontal regions, and are preferentially lateralized to the right. Several studies found regions that were
755
similarly activated by recognition across age groups (Daselaar et al., 2003; Tisserand et al., 2005), leading
756
researchers to suggest that age effects are more pronounced for encoding than retrieval. However, age-
757
differences are still seen in the latter. Several studies found decreased activity in the right PFC in older adults
758
(e.g., Anderson et al., 2000; Cabeza et al., 1997; Bäckman et al., 1997); this frontal under-activation was greater
759
for source recall tasks than for recognition tasks, suggesting that reductions in right frontal activity might be
760
proportional to the difficulty of the task. Whereas the left
761
anterior PFC regions are more strongly involved in retrieval (Spaniol, 2009). Sub-regions of the PFC have been
762
implicated in various retrieval-related functions, including setting the retrieval mode, specifying retrieval cues,
763
and post-retrieval monitoring and verification (e.g., Burgess et al., 2007; Cabeza et al., 2003; Dobbins and Han,
764
2006; Moscovitch and Winocur, 2002; Rugg et al., 1998; Shallice, 2002; Simons and Spiers, 2003). The first two
765
aspects are more dependent on the
766
DL
767
in older subjects compared to young subjects. In addition, various frontal sub-regions have been demonstrated to
768
be differentially involved in recollection (R) and familiarity (F) (for review, see Skinner and Fernandes, 2007).
769
Both have been associated with right
770
the anterior frontal (related to source information) and superior frontal (related to attentional processes) regions.
771
In the future, it should be interesting to determine how the frontal lobe sub-regions contribute to different
772
processes related to R- and F-based responses.
773
VLPFC,
VLPFC
was more strongly involved in encoding,
whereas monitoring and verification are more dependent on the
PFC. Schacter et al. (1996) found that frontal activity during recall of word pairs was located more posteriorly
DLPFC
activity, while R is associated with additional bilateral activity in
4.5/ Medial temporal lobes
774
Following Scoville and Milner’s (1957) report on amnesic patient HM, human and animal lesion work
775
focused intensively on the role of the hippocampus and surrounding MTL in memory (for review, see Annese et
776
al., 2014; Rosenbaum et al., 2014). Vargha-Khadem et al. (1997; 2001) noted that severe EM disorders were
777
associated with congenital bi-hippocampal lesions. This structure operates by forming associations among the
778
sensory, cognitive and emotional processes that make up an episode in memory (Eichenbaum, 1996; see also
779
Hannula et al., 2006; Holdstock et al., 2005). The MTL has been the subject of much research in this area, both
780
because it plays a key role in EM function (for reviews, see Cabeza and Nyberg, 2000; Desgranges et al., 1998)
781
and because it is usually the first structure targeted by AD lesions (for review, see Dickerson and Eichenbaum,
782
2010). This structure seems to be involved in novelty detection (e.g., Dolan and Fletcher, 1997), and in encoding
21
783
and conscious retrieval of information (Wheeler et al., 2004). Notably, more severe age-related declines have
784
been associated with decreased activity in the MTL during encoding (Daselaar, 2003; Spaniol, 2009; Tisserand
785
et al., 2005).
786
The left-sided activation of the temporal and cingulate areas in encodingtasks reflects an asymmetrical
787
activation that fits the HERA model, but also seems to depend on the material in question (Desgranges et al.,
788
1998). For example, MTL is bilaterally activated during the encoding of digitized topographic information
789
(Aguirre et al., 1996), and the intentional encoding of complex images (Stern et al., 1996), while right
790
hippocampal activation was observed during face learning (Grady et al. 1995). Indeed, the results for this
791
structure are divergent. Some studies have found atrophy of the hippocampal region (Tisserand et al., 2004), and
792
less activity during memory encoding (Spreng et al. 2010) and retrieval in the elderly compared to young healthy
793
subjects (Dennis et al., 2007; Gutchess et al., 2005; Morcom et al., 2003; St Jacques et al., 2009). Decreased
794
medial-temporal involvement among elderly subjects has been reported in a number of tasks, including the
795
encoding of faces (Grady et al., 1995), verbal materials (Daselaar et al., 2003) and natural scenes (Park et al.,
796
2003). Age-related under-recruitment is believed to contribute to the age-related deficits observed in EM
797
performance. For example, when Daselaar et al. (2003) divided older adults according to their performance, low
798
performers showed less hippocampal activity than high performers. Moreover, reduced MTL function is often
799
accompanied by increased activation in the frontal cortex (i.e., PASA). Other studies have shown a relative
800
preservation (Good et al., 2001 Miller et al., 2008; Persson et al., 2011; Sullivan et al., 2005) and left MTL
801
activation during encoding was shown to predict successful memory retrieval performance in both young and
802
older subjects (Bernard et al., 2007). The apparent discrepancies in such results may reflect the encoding process
803
used. For example, Grady et al. (1999) observed bilateral recruitment of MTL regions when they focused on
804
subsequent memory, whereas Spreng et al. (2010) studied episodic encodingand noted reduced activity in the
805
right MTL of older adults. Alternatively (or in addition), the age range of the selected subjects may explain the
806
between-study differences: for samples covering a wide age range, the results tend to favor the preservation of
807
the structure, whereas studies focusing on narrower age ranges, especially patients over 50 or 60 years, found
808
atrophy of the hippocampus (for review, see Barbeau, 2011).
809
Based on the finding that elderly adults typically benefit less than young adults from deep processing of
810
study items, age-related impairments in EM are believed to be related to deficiencies in semantic processing
811
during encoding. For example, Daselaar et al. (2003) used fMRI on groups of young and elderly adults,
812
comparing brain activity patterns obtained during deep (living/non-living) and shallow (uppercase/lowercase)
813
encoding tasks. Although other regions were commonly activated during both processes, older adults revealed
814
significantly less activation in the left anterior hippocampus during deep processing but not shallow processing
815
compared to the young. This suggested that deep processing activates the MTL in young subjects but not older
816
subjects, further suggesting that there may be an age-related dysfunction of the posterior portion of the
817
hippocampus (Kalpouzos et al., 2008).
818
The findings from PET studies converge to the observations made by Lepage et al. (1998), who stated
819
that episodic encoding is almost exclusively associated with the anterior caudal region of the MTL, particularly
820
the hippocampus, whereas more posterior rostral (though not necessarily hippocampal) MTL regions play a
821
stronger role in episodic retrieval. Thus, the hippocampus may not function exclusively in the encoding or
822
recalling of events. For both encoding and retrieval, neural activations are located preferentially in the left
823
hemisphere for verbal material and in the right or both hemispheres with non-verbal stimuli (Davachi, 2006).
824
This rostro-caudal gradient, which is referred to as the HIPER (HIPpocampal Encoding/Retrieval) model,
22
825
(Lepage et al., 1998) seems to hold for verbal and non-verbal materials, and largely for both hemispheres too,
826
especially during retrieval, when the activations produced by the two stimulus types are distributed more or less
827
evenly in both hemispheres. The situation is less clear for the encoding of verbal information, as researchers
828
noted an absence of associated activation in the right hippocampal region. Furthermore, some studies have failed
829
to support the distinction of an anterior-posterior gradient. For example, Greicius et al. (2003) found that the
830
middle and posterior parts of the hippocampus are associated with both the encoding and retrieval of episodic
831
information. Moreover, other studies contradicted that of Lepage by showing that: 1) the anterior part of the
832
MTL is more strongly involved in retrieval, whereas the posterior part is associated with encoding processes
833
(Gabrieli et al., 1997; Rombouts et al., 2001; Schacter & Wagner, 1999); and 2) encoding activations in PET are
834
observed frequently in both anterior and posterior MTL sites, with a less clearly defined tendency for a
835
rostrocaudal gradient. In light of these results, it is then important to determine why episodic encoding involves
836
both the anterior and posterior MTL, whereas episodic retrieval is mainly associated with the posterior region
837
(Madden et al., 1999). In general, age-related changes in MTL activity are consistent with the associative deficit
838
theory, which posits that age-related memory deficits primarily reflect difficulties in encoding and retrieving
839
novel associations between items (Chalfonte and Johnson, 1996; Naveh-Benjamin, 2000;). Given that relational
840
memory has been strongly associated with the hippocampus, this hypothesis predicts that older adults will show
841
decreased hippocampal activity during memory tasks, particularly tasks that involve associations.
842
Some authors have favored the idea that the medial temporal cortex mainly functions in the recall of
843
episodic information (Ekstrom and Bookheimer, 2007), while other studies have contradicted this notion
844
(Cabeza et al., 1997). According to Schacter et al., (1996), the absence of hippocampal activation in some
845
studies seems to be related with the nature of the utilized tasks, with primary involvement of the PFC observed
846
when the task requires a highly demanding research strategy. The involvement of the hippocampus has been
847
demonstrated during the retrieval of episodic information with respect to verbal material (Rugg et al., 1997;
848
Schacter et al., 1996), drawings (Schacter et al, 1995), and topographical information (Owen et al., 1996). A
849
growing body of literature describes the neural structures underling recollection and familiarity in healthy
850
individuals. Within the MTL, studies have distinguished between the hippocampus and the parahippocampal
851
gyrus (Shastri, 2002): the former appears to be related to both recollection and familiarity (Aggleton and Brown,
852
1999; Mayes et al., 2002), and is reduced in older adults; the latter, in contrast, is related to familiarity and shows
853
increased activity in the elderly relative to younger subjects (Bäckman et al., 1997; Daselaar et al., 2006; Skinner
854
& Fernandes, 2007; Yonelinas, 2001; but also see Stark and Squire, 2003). This conclusion is supported by the
855
R/K paradigm, wherein subjects must specify under which circumstances the information was encoded (i.e., with
856
or without revival). Hippocampal activation is lower in the elderly compared to younger subjects, reflecting the
857
importance of the hippocampus in the more elaborate aspects of EM. In contrast, the rhinal and perirhinal
858
cortices (located near the hippocampus) show greater activity in older subjects, suggesting that this region
859
underpins another, less fragile aspect of memory: the feeling of familiarity (Daselaar et al., 2006; Vanssay-
860
Maigne et al., 2011). These results are in line with the fact that elderly people show greater impairments in
861
recollection than in familiarity (e.g., Cabeza et al., 2004; Jennings and Jacoby, 1993; but also see Rosenbaum et
862
al., 2014, patient NB), and suggest that the elderly rely more heavily on familiarity to compensate for the deficit.
863
These findings also indicate that older adults compensate for hippocampal deficits by relying more on the rhinal
864
cortex, possibly through a top-down frontal modulation. This is consistent with the fact that older people present
865
a larger portion of “Know” responses than younger adults. In sum, during episodic retrieval, both decreases and
866
increases in MTL activity may be seen, depending on the involved sub-region(s).
23
867
4.6/ Are other neural substrates of EM affected by age?
868
In addition to the PFC and MTL regions, neuroimaging studies have also implicated the parietal cortex,
869
the cingulate gyrus, the retrosplenial region, the amygdala and the cerebellum in EM (Desgranges et al., 1998;
870
Spaniol, 2009). The effects of aging on these brain structures have not yet been established, but the parietal
871
neocortex has been increasingly accepted as being involved in the age-related declines of EM (Desgranges et al.,
872
2008; for review, see Wagner et al., 2005). As proposed Nyberg et al. (1996) with respect to young subjects, the
873
asymmetry described by the HERA model may hold true for other brain regions, becoming a “HERA extended”
874
model. The encoding of episodic information activates the left parietal cortex during object localization, and
875
Sperling et al. (2003) found that parietal activation during the encoding of novel face–name pairs was higher in
876
elderly participants versus young controls. In contrast, however, bilateral or right-side activations of the parietal
877
cortex have been associated with retrieval (Desgranges, 1998). In a category-learning task, older adults showed
878
greater bilateral parietal activation compared to young adults, and this bilateral activity was associated with
879
higher performance (Fera et al., 2005). This age-related over-recruitment also appears to be compensatory,
880
perhaps improving the ability of older adults to resolve tasks. In their meta-analysis, Maillet and Rajah (2014)
881
noted that the regions that are over-recruited by older adults during successful encoding all overlap with or occur
882
in close proximity to regions that have been associated with encoding failures in young adults. In a recent study,
883
when performing a Stroop-like task (i.e., identifying number magnitude and physical size), Huang et al. (2012)
884
observed that the left posterior parietal cortex (PPC) and right parietal cortex are recruited in young subjects
885
asked to identify number magnitude, while the right and left PPC were both recruited when these subjects were
886
asked to judge physical size, supporting the existence of compensatory processes in normal aging (see also
887
Nielson et al., 2002). These observations suggest that the HAROLD model may apply to regions other than the
888
PFC (Collins and Mohr, 2013).
889
The research has largely focused on the lateral parietal region, as damage to this region impairs some
890
aspects of EM(e.g., Davidson et al., 2008). The lateral parietal region may be activated during encoding and
891
retrieval (e.g., Ciaramelli et al., 2008), depending on the utilized material and studied sub-region, but it seems to
892
be more strongly associated with successful retrieval than successful encoding (for review, see Olson and
893
Berryhill, 2008). The encoding and retrieval of EM information requires some level of attention (e.g., Anderson
894
and Craik, 1974; Carrasco et al., 2004; Fernandes and Moscovitch, 2000; Moscovitch, 1992), which may depend
895
in part on the parietal cortex. Cabeza et al. (2008) proposed an anatomical model of memory and attention (the
896
Attention to Memory model), in which retrieval depends on distinct regions of the lateral PPC (Cabeza et al.,
897
2011;Naghavi and Nyberg, 2005; Spaniol, 2009). Indeed, parietal damage can impair the conscious retrieval of
898
even well encoded information (Bisiach and Luzzatti, 1978). The dorsal PPC region directs attention towards a
899
retrieval goal, whereas ventral PPC regions are implicated in bottom-up attention, as captured by environmental
900
stimuli or sensory cues. Distinctions can also be made between the superior and inferior parietal regions, which
901
show complementary patterns of activity: the superior area appears to reflect top-down influence in mediating
902
low-confidence responses, while the inferior region reflects a bottom-up influence that mediates high-confidence
903
responses (Kim and Cabeza, 2007). Studies have shown that different parietal regions are differentially involved
904
in various processes related to retrieval (Vilberg and Rugg, 2008). In fMRI studies using the R/K paradigm,
905
parietal activations were found to be stronger for items accompanied by vivid, clear recollections compared to
906
those accompanied by a feeling of knowing (Henson et al., 1999; Skinner and Fernandes, 2007; Wheeler and,
907
2004; for review, see Wagner et al., 2005). The dorsal parietal cortex is believed to support familiarity, whereas
24
908
the ventral region is concerned with recollection. Within the cortex, the temporo-parietal region contributes to
909
recollection, while the occipito-parietal region is associated with familiarity (Daselaar et al., 2006).
910
Another structure that has been highlighted as playing a role across a range of cognitive functions
911
(including EM) is the cerebellar region. The effects of aging on this structure are less well understood, however,
912
as no study has yet compared its activation between young and old people. Schacter et al. (1996) proposed that
913
(similar to the PFC) the cerebellum might be involved in strategic processes, retrieval efforts and the inhibition
914
of irrelevant information. Andreasen et al.(1995) underlined the close anatomical connections between the
915
cerebellum and the PFC, and suggested that (similar to the left PFC) the right cerebellum might belong to a
916
general memory circuit involved in the encoding of information. However, the data are inconsistent across
917
studies. Cerebellar activations were reported only for verbal materials and showed a tendency for right
918
lateralization during encoding tasks in some studies (Cabeza and Nyberg, 2000; Fliessbach et al., 2007), while
919
others have found that activation of the cerebellum appears to favor retrieval over encoding, and to
920
predominantly concern the left cerebellar hemisphere (Desgranges et al., 1998; Wiggs et al., 1999). Further
921
studies are needed to elucidate any age-related differences and to understand the specific role of the
922
cerebellum.The MRI- and PET-based study of age-related structural and functional changes performed by
923
Desgranges et al. (2008) showed that the most highly deteriorated morphological structures include the frontal
924
and parietal cortices, and the more caudal aspect of the hippocampal regions. The best-preserved regions, in
925
contrast, include the rostral hippocampal regions and the thalamus, especially the lateral nuclei. At the functional
926
level, the frontal and parietal cortices are the most sensitive to the effects of aging, followed by the MTL, while
927
the other regions are preserved. These results are consistent with the developmental hypothesis, which states that
928
the brain regions that develop first are the most resistant to the effects of aging, whereas the regions that develop
929
last are the most fragile.
930
While the above-described overview of the main involved anatomical structures provides insight into
931
their declines in normal aging, an emerging (yet consistent) finding in memory research is there are also age-
932
related differences in the functional connectivities of brain regions. Close anatomical linkages between the
933
parietal, occipital, frontal and medial temporal lobes have been shown to support EM encoding and retrieval
934
(Olson and Berryhill, 2009). During EM, age differences have been observed in studies that measured brain
935
activity during the successful encoding of words (Dennis and Cabeza, 2008), scenes (St Jacques et al., 2009) and
936
objects (Addis et al., 2010) with the Dm effect paradigm. During successful encoding, the elderly have a weaker
937
functional connectivity between the MTL and posterior regions (i.e., the occipital or parietal cortices), but
938
greater connectivity between the MTL and PFC, as compared to younger adults (Daselaar et al., 2006; Dennis et
939
al., 2008; Hayes et al., 2008; Leshikar et al., 2010; Park & McDonough, 2013). Some authors have found age-
940
related reductions in the fronto-temporal network during memory encoding (Grady et al., 1995; Grady et al.,
941
2003; Wang et al., 2010;), while altered fronto-occipital connectivity has also been observed with increasing age
942
(Moeller et al., 1996). Cabeza et al. (2004) found that older adults showed decreases in parietal and occipital
943
regions coupled with increases in PFC regions. Age-related differences in functional connectivity have also been
944
found during retrieval, most notably in temporal-parietal connectivity during recognition tasks. Using a verbal
945
task, Daselaar et al. (2006) demonstrated that older adults had reduced frontal connectivity within a
946
hippocampal–parietotemporal network relative to young adults, but increased connectivity within a
947
parahippocampal–frontal network. This result was interpreted as indicating that older adults compensate for
948
hippocampal deficits by relying more on the parahippocampal cortex. This is consistent with the notion that
25
949
older adults globally compensate for decreases in the neuronal activity of one brain region by recruiting
950
additional resources to perform a cognitive task (Dennis and Peterson, 2012; Davis et al., 2008).
951
In conclusion, EM is assembled in a complex circuit. Neurocognitive models of EM postulate that the
952
strategic component of the observed deficit depends primarily on the PFC, whereas the associative component
953
mostly relies on the MTL, especially the hippocampus (e.g., Simons and Spiers, 2003; Shing et al., 2010 for
954
reviews; Shing and Lindenberger, 2012). Along with the parietal cortex, these are key structures in both
955
encoding (Rombouts et al., 1997; Stern et al., 1996) and retrieval (e.g., Shannon and Buckner, 2004; Dennis and
956
Cabeza, 2008) of EM. Although little explored, EM deficits in older adults can also be related to age-related
957
differenceswithin the same group, between individuals, and according to single or multiple factors. Those same
958
factors might also be responsible for the accelerated declines seen in the most important neurodegenerative
959
diseases (i.e., AD), and may help direct the onset of the symptoms and the intra-individual differences that can
960
be seen between two people at the same stage of the disease.
961
5/ Inter-individual variability associated with EM in normal aging and Alzheimer disease
962
5.1/ Lifestyle
963
Age affects EM performance among healthy individuals (Kramer et al., 2003), but there are clearinter-
964
individual variabilities (Christensen et al., 1999; Morris and Price, 2001; Raz et al., 2009): while some people
965
decline rapidly and experience severe memory impairment at a relatively young age, even to the point of being
966
diagnosed with dementia, others undergo“normal” or even “successful” aging with little change (or even some
967
improvement)in their mental capacity into extreme old age (Albert et al., 1995; Dixon and de Frias, 2014; Reed
968
et al., 2010; Rubin et al., 1998; Wilson et al., 2002; Zelinski et al., 1993).When cognitive capacities decline in
969
aging, and particularly AD, EM is one of the first systems to fail (Hodges, 2000). Longitudinal studies have
970
confirmed that individual differences in cognitive performance increase from early to late adulthood (e.g., de
971
Frias et al., 2007); a number of individual characteristics have been found to be critically associatedwith the
972
variances in this process, and thusmay contribute to modulating the effects of aging on cognitive functions
973
(Anstey and Christensen 2000; Lemaire and Bherer, 2005). Two major negative factors are obesity
974
(e.g.,Sellbomand Gunstad, 2012) and hypertension (e.g.,Etgen et al., 2010; Raz and Rodrigue,2006; see also
975
Deary et al., 2009), and environmental and genetic influences also appear to be involved (e.g., Deary et al.,
976
2009;Finkel et al., 2005; McGue et al., 1993).Colombes et al. (2006) and Stern (2002) showed that the negative
977
effects of aging could be slowed throughout life (including in centenarians)bythe protective effects derived from
978
continuous cognitive stimulation, whichcontributesto thecognitive reserve (CR).In addition,heritability studies
979
have indicated that genetic variants strongly influence differences in cognitive ability throughout the lifespan,
980
including in old age (e.g., Tupler et al., 2007; Mormino, 2014)
981
The concept ofreserve (both passive and cognitive), which provides a framework for explaining
982
individual-level characteristics (Stern, 2011), reflects the amount of damage that can be sustained before
983
reaching a critical threshold at which clinical signs manifest (Bastin et al., 2013; Brickman et al., 2011;
984
Kalpouzos et al., 2008; Nyberg et al., 2012; Satz, 1993).The passive reserve refers to differences in brain
985
structure, such as neuronal density (Villeneuve and Belleville, 2010), which may increase the brain’s tolerance
986
of disease. This brain reserve differs from the CR, which Stern (2002, 2009) defined as an individual’s ability to
26
987
optimize or maximize performance on cognitive tasks by recruiting the same or different (neural compensation)
988
brain networkscompared to young subjects, and thus using alternative cognitive strategies (Baldivia et al., 2008).
989
The CR hypothesis posits that at any given level of clinical severity, the underlying pathology of AD is more
990
advanced in patients with a higher level of CR (Vemuri et al., 2011). IQ (e.g.,Christensen et al., 2007; Willerman
991
et al., 1991), social interactions (e.g., Fritsch et al., 2007; Scarmeas and Stern, 2003), leisure activities [both
992
cognitive (Fratiglioni et al., 2004; Fritsch et al., 2007; Stern, 2006) and physical (Anstey and Christensen, 2000;
993
Nithianantharajah and Hannan, 2009; Smith et al., 2014)], level of education (Andel et al., 2006; Bruandet et al.,
994
2008; Christensen et al., 2009; Fritsch et al., 2002; Singh-Manoux et al., 2011; Vance et al., 2010),and
995
professional activities (e.g., Andel et al., 2006; Fritsch et al., 2002)confera lifelong set of skills that maylengthen
996
an individual’s resistance against age-related cognitive declines and reduce his or her risk of
997
developingAlzheimer’s disease(for review, see alsoScarmeas and Stern, 2003; Valenzuela and Sachdev, 2006).
998
Alzheimer's patients with a high CR but a more advanced disease stagecan operate at a level of clinical severity
999
equivalent to that of lower CR patients in earlier stages of the disease.However, such patients show greater AD-
1000
related brain damage (i.e., parieto-temporal and frontal hypoperfusion)andonce the cognitive decline begins in
1001
such individuals, it progresses more quickly than in other groups (Hall et al., 2007; Figure 3). Scarmeas et al.
1002
(2004) demonstrated that the hippocampus plays an important role in the reservesof AD patients, assignificant
1003
activation of this structure seems to be the optimal response in AD patients with high CR.
1004 1005 1006
- Insert Figure 3 about here –
1007 1008
1009
5.2/ Genetics
1010
Although lifestyle factors can help people grow older successfully, new research has also focused on the
1011
roles played by genetic differences, especially given that EM is a heritable and polygenic trait
1012
(Papassotiropoulos and de Quervain, 2011). In normal populations(Plomin et al., 2001; Plomin and Spinath,
1013
2002; Friedman et al., 2008), including twin and adoption studies (Bouchard and McGue, 1981; Bouchard and
1014
McGue, 2003; Carmelli et al., 1997; Petrill et al., 2001), over 50% of the variance in adult cognitive ability is
1015
thought to arise from genetic influences. In recent years, researchers have linked specific genes (COMT, BDNF,
1016
ApoE4 for the main) to cognitive functioning and EM in older adults (Goldberg and Weinberger, 2004; Harris
1017
and Deary, 2011), as well as many of the dementias that have been seen in older populations.
1018
As a variety of evidence has implicated the PFC and dopaminergic pathways in cognition and EM (e.g.,
1019
Dickinson and Elvevag, 2009; for review,see Lisman and Grace, 2005; Shohamy and Adcock, 2010), some
1020
researchers have focused on genes that are related to the regulation of dopaminergic function. Evidence suggests
1021
that the relationship between DA levels and prefrontal cognitive performance follows an inverted-U-shaped
1022
function, where performance is impaired by the presence of too little or too much DA (Mattay et al., 2003; for
1023
review, see Cools andD’Esposito, 2011).Catechol-O-methyl transferase (COMT) is an enzyme that inactivates
1024
the release of DA (Raz et al., 2009). Humans havea functional polymorphism in the COMT gene, where a
27
1025
methionine (Met) for valine (Val) substitution at codon 158 (Val158Met) reduces the enzyme’s thermostability
1026
and activity (Chen et al., 2004; Lewis et al., 2001; Mazei et al., 2002; Moron et al., 2002), thereby decreasing the
1027
degradation of DA in the neocortex. The high-activity Val allele, in contrast, directs faster catabolism of
1028
prefrontal DA at the synapse, impairing prefrontal function and reducing performance on a range of cognitive
1029
tasks among Val carriers compared to non-Val carriers (e.g., Egan et al., 2001). COMT has been mainly
1030
associated with executive functions in studies of both younger and elderly individuals (Payton, 2009), with
1031
homozygotes for the low-activity Met allele performing better than subjects with the high-activity Val allele
1032
(Malhotra et al., 2002; for review, see also Greenwood andParasuraman, 2003). De Frias et al. (2004) found an
1033
association of this functional polymorphism with EM, with Met/Met carriers outperforming the Val carriers, as
1034
found by Bates et al. (2003) on a delayed visual memory-recall task (see also Savitz et al., 2006 for a
1035
review).However, a meta-analysis yielded mixed results, including little to no association between the COMT-
1036
Val158Met genotype and cognitive function (Barnett et al., 2008).
1037
The gene encoding brain-derived neurotrophic factor (BDNF) has been associated with EM
1038
performance (de Quervain et al., 2003; Egan et al., 2003; Ho et al., 2006; Voineskos et al., 2011; see also
1039
Papassotiropoulos and de Quervain, 2011 but see Harris et al., 2006; Dennis et al., 2011; Laing et al., 2012;
1040
Gong et al., 2012 for inconsistent findings) and appears to play a role in the MTL, primarily in the hippocampus
1041
(Greenwood andParasuraman, 2003; Hariri et al., 2003; Kambeitz et al., 2012), but also in the PFC (Bertolino et
1042
al., 2006; Pezawas et al., 2004) in humans and non-human species. A steady decline in BDNF expression has
1043
been associated with normal aging (Tapia-Arancibia et al., 2008), while in AD,its expression is reduced in the
1044
hippocampus and entorhinal cortex (i.e., the first structures to be pathologically degraded).This neurotrophin has
1045
been linked to the long-term potentiation-mediated facilitation of memory formation (Poo, 2001). A common
1046
functional Val-to-Met substitution at amino acid 66 (Val66Met) has been identified, with the Met allele
1047
associated in some studies with impaired BDNF trafficking and poorer EM performance (e.g., Hariri et al., 2003;
1048
Kambeitz et al., 2012), while other studies reported contradictory results (Harris and Deary, 2011; Dennis et al.,
1049
2011). Nevertheless, behavioral results from Egan et al. (2003) showed that the BDNF polymorphism is
1050
associated with delayed recall of stories but not word lists, suggesting a different involvement according on the
1051
task. Furthermore, Met carriers appeared to exhibit poorer performance (Koppel and Goldberg, 2009) and
1052
reduced neural activity within the MTL when performing EM tasks(Bath and Lee, 2006; Bueller et al., 2006;
1053
Hairi et al., 2003;Kauppi et al., 2014). The Met BDNF allele is associated withabnormal hippocampal function
1054
and greater prefrontal activity (Mattay et al., 2008). This may reflect the presence of a compensatory mechanism
1055
that can maintain performance and decreased EM performances in elderly subjects and young healthy
1056
individuals compared to BDNF Val homozygotes (Pezawas et al., 2004).Voineskos et al. (2011) showed that
1057
elderlyVal homozygoteswere characterized by decreases in EM performance, entorhinal cortex thickness,
1058
andintegrity of the white matter tract. Additionally, functional brain imaging studies indicated that Met carriers
1059
exhibit higher MTL activity than non-Met carriers during both encoding and retrieval ofEM tasks (Dennis et al.,
1060
2011), even when the analysis controlled for cognitive performance. The authors suggested that this increased
1061
activity might be needed to match the memory performance of non-carriers. The possible interaction ofthe
1062
COMT and BDNF polymorphisms has been examined. For example, Miller and Cohen (2001) proposed that the
1063
two factors might jointly regulate the prefrontal-MTL circuit responsible for EM,while Nagel et al. (2008) found
1064
an interaction between BDNF Val66Met, COMT Val158Met, and age. The latter authors posited that older
1065
individuals homozygous for the Val allele of COMT experienced additional performance declines if they were
1066
also BDNF Met-carriers, suggesting that the BDNF polymorphism negatively modulates the interaction between
28
1067
age and Val-COMT. Moreover, Witte et al. (2012) reported that the interaction between these COMT and BDNF
1068
polymorphisms explained significantly more of the variation in cortical plasticity than either gene alone.
1069
Finally, a functional polymorphism in the gene that encodes apolipoprotein (ApoE) is the most clearly
1070
established genetic risk factor for AD (for review, see Grady, 2012). ApoE is a ubiquitous protein that plays a
1071
major role in the clearance of beta-amyloid (A), which is thought to be the neurotoxic agent of AD. The
1072
encoding gene has three allelic variations in the human population:2, 3, and 4. In contrast to 2 and 3
1073
carriers, 4 allele carriers are at adose-dependently increasedrisk for developing AD (Havlik et al., 2000;
1074
Katzman et al., 1997; Moffat et al., 2000; Perry et al., 2001), with two copies of 4 increasing the risk of
1075
developing early AD to 80%, compared toa risk of 20% in the absence of the allele (Corder et al., 1993; for
1076
ameta-analysis, see Farrer et al., 1997). Compared to the heterozygous carriers, 4 homozygotes have greater
1077
deficits in EM tasks (e.g., Nilsson et al., 2006; Matura et al., 2014), even when such individuals are selected as
1078
“high functioning” (Bretsky et al., 2003); they also show reduced bilateral MTL volumes (Lemaître et al.,
1079
2005).However, 4-carrier status is associated with greater longitudinal declines in memory performance, which
1080
become evident by the sixth decade of life (Caselli et al., 2009). A recent study by Kantarci et al. (2012) showed
1081
for the first time that the ApoE genotype modifies the association between cognition and the A load, which is
1082
measured with PIB-Pittsburgh compound B andconstitutes the senile plaques in cognitively normal older adults
1083
(see also Sparks et al., 1996). While PIB retention was modestly associated with cognitive function even after
1084
the data were adjusted for age, sex, and education, the presence of the ApoE 4 allele significantly increased the
1085
A load and influenced the relationship between the A load and cognitive function, increasing the risk of
1086
cognitive decline in healthy individuals. Another tracer (18F-FDDNP) was used by Shoghi-Jadid et al. (2002) to
1087
label bothNFT(Neurofibrillary tangles) and A deposits, the main proteins that misfold and accumulate in AD.
1088
The authors found significant accumulation of this marker in the hippocampal region, a strong link between
1089
marker fixation areas and hypometabolism areas,and a negative correlation between marker accumulation and
1090
EM. Kauppi and colleagues (2014) recently investigated the combined effect of APOE and BDNF on
1091
hippocampal activity and found thatthe APOE 4 and BDNF Met alleles were associated with decreased
1092
activation of the anterior (hippocampus) and posterior (parahippocampal gyrus) parts of the MTL(see also Ward,
1093
2014; conversely, see Richter-Schmidinger et al., 2011). Faster EM declines and reduced hippocampal
1094
volumeswere found in Met carriersof BDNF with high A loads among those in the prodromal stage of AD (Lim
1095
et al., 2014). However, it is important to emphasize that the ApoE 4 allele appears to have only a limited effect
1096
on cognition in dementia-free individuals (e.g., Small et al., 2000). In a recent study, Ferencz et al. (2013) did
1097
not find that ApoE alone affected hippocampal (HC) volume and EM performance in adults older than 60
1098
years;however, they did observe an association between HC volume and free recall performance in ApoE 4
1099
carriers who also carried the risk alleles of TOMM40, which encodes a protein that is required for transporting
1100
proteinsinto mitochondria. On a functional level, PET studies revealed widespread reductions in the glucose
1101
metabolism of cognitively intact adults (50-65 years old) (Reiman et al., 1996),and in younger adults carrying
1102
the 4 allele (20-39 years old, Reiman et al., 2004), as assessed in the posterior cingulate, temporo-parietal and
1103
prefrontal regions (i.e., the same regions that exhibit metabolic deficits in AD patients) (Alexander et al., 2002).
1104
These observations suggest that the neural networks that sub-serve EM function are altered in APOE 4 carriers
1105
in a manner similar to that observed in subjects with early dementia (i.e., MCI; Bookheimer et al., 2000).
1106
Additionally, healthy ApoE 4 carriers show volume reductions in the hippocampus (Cohen et al., 2001; Moffat
29
1107
et al., 2000), the white matter (Plassman et al., 1997) and the gray matter in the medial temporal and fronto-
1108
temporal regions (Wishart et al., 2006), compared to non-carriers. However, a study by Han and colleagues
1109
(2007) found that multiple right hemisphere brain regions were activated more strongly during a verbal paired-
1110
associated learning task in ApoE 4 non-demented older adults compared to their non-4 counterparts. The
1111
authors suggested that at-risk personsmight require additional structures to maintain a level of behavioral
1112
performance equivalent to that of non-4 allele carriers.
1113
In sum, the existence of a large inter-individual variation in performance and neuronal substrate has often
1114
been reported in the literature and this variability even seems to increase with age. Several characteristics appear
1115
critical in the appearance of these interindividual differences, including environmental, genetic and “self”
1116
(education, activities…) factors. The emotional state of the subjects and the congruence of this state at the time
1117
of encoding and recall might also influence this variability (Syssau, 1998 for review). With the existence of these
1118
risk factors, how EM decline is seen in Alzheimer disease?
1119
6/ Episodic memory and Alzheimer disease
1120
6.1/ Pathophysiology and characteristics of the disease
1121
AD is a progressive, irreversible and severely disabling disorder of memory and cognition that inevitably
1122
results in the need for intensive care, and ultimately indeath. Initially discovered by Aloïs Alzheimer in 1906,
1123
AD is a neurodegenerative disease of the central nervous system. The disease is characterized by two types of
1124
microscopic brain lesions, amyloid plaques (or senile plaques; Gouras et al., 2000) and neurofibrillary tangles
1125
(NFT; Grundke-Iqbal et al., 1986), along with neuronal and synaptic loss. Amyloid plaques arise from the
1126
extracellular accumulation of Aß protein (a metabolic waste product), whileNFTreflect accumulation of the tau
1127
protein, which is inactivated by hyper-phosphorylation and found as conglomerates in the cell body of the
1128
neuron and its extensions. The microscopic lesions lead to neuronal dysfunction and death, yielding the
1129
macroscopic result of altered brain activity and cortical atrophy, with the brain losing about 8-10% of its weight
1130
within a decade. In vivo neuroimaging techniques (i.e., MRI and PET) have revealed that this atrophy first
1131
develops in the MTL, entorhinal cortex and hippocampus (Schwindt and Black, 2009), andthen spreads into the
1132
neocortex (Delacourte et al., 1999), followed by thesubcortical nuclei, brainstem and cerebellum (Thal et al.,
1133
2002).
1134
In the absence of any clear biological or neurological marker, AD is also characterized by cognitive deficits
1135
that gradually affect overall cognitive functioning. Of the five major memory systems, most authors consider the
1136
EM system to be the most clinically relevant for AD patients (e.g.,Bäckman et al., 2004; Dubois et al., 2007;
1137
McKhann, 2011;Small and Bäckman, 2007; Thomas-Anterion and Laurent, 2006),given that impairments in this
1138
system can worsen memory for recent events, leading to functional deficits. AD has a preclinical period called
1139
MCI (Mild Cognitive Impairment), during which early and mild cognitive deficits can be identified (e.g., Bordet
1140
et al., 2010); in 50% of affected individuals, this period evolves to AD pathology within a few years
1141
(Trojanowski et al., 2010). Although MCI may therefore represent a prodromal stageof AD, it is a heterogeneous
1142
syndrome, with some patients never progressing to dementia (Richard and Brayne, 2014).
30
1143
6.2/ Behavioral data
1144
Patients with AD show deficits in EM from the very early stages of the disease. These performance deficits
1145
reflect disorders of encoding andstorage (e.g., Pena-Casanova et al., 2012) but also retrieval. These disorders are
1146
often associated with temporal and spatial disorientation, and patients often have difficulties withEM tasks (for
1147
review, see Ergis& Eusop-Roussel, 2008). In memory consultations for the early detection of dementia, one of
1148
the most widely used tests for assessing EM is called “free recall-cued recall 16 items” (Desgranges and
1149
Eustache, 2003).This test aims to differentiate EM pure disorders from apparent memory deficits. Whereas pure
1150
memory disorders are due to problems with encoding or consolidation, underpinned by the hippocampus,
1151
apparent memory deficits are related to the use of inefficient strategies, attentional disorders that affect memory
1152
performance, and information-retrieval disorders, underpinned by the frontal cortex (Eustache et al., 2006).This
1153
verbal test, developed by Grober and Buschke (1987) is based on the encoding depth (the subject is asked to
1154
perform semantic processing of presented words) and encoding specificity (the same clues are used during
1155
encoding and recovery, and the effectiveness of retrieval cues depends on the conditions under which the
1156
information was encoded). In AD, the obtained pattern largely favors an encoding disorder, with AD patients
1157
having difficulties with establishing an elaborate (deep semantic) encoding of either the target information or the
1158
context (e.g., Bird and Luszcz, 1991; Bondi and Kaszniak, 1991; Monti et al., 1996) compared to healthy older
1159
people. Moreover, AD patients have performance deficits in both recall and recognition, leading some
1160
researchers to posit the presence ofan encoding deficit (Delis et al., 1991; Bäckman and Small, 1998). Dalla
1161
Barda and Goldblum (1996)found that the recognition performances of their non-healthy participantswere lower
1162
than those of the control group, and patients were less capable of correctly associating items by their semantic
1163
relationships (see also Goldblum et al., 1998). Similar to AD patients, MCI subjects gain little benefit from the
1164
semantic links that would normally be used during the encoding of words (Perri et al., 2005). This difficulty
1165
could reflect either an inability to discriminate between two related concepts due to loss of the details
1166
distinguishing the concepts (e.g., Martin and Fedio, 1983; Sailor et al., 1998) or an inability to relate those
1167
concepts during encoding. Moreover, some authors have observed that patients are unable to retrieve information
1168
when the recall task is delayed (e.g., Hart et al., 1988), suggesting that there is a deficit in the consolidation of
1169
information during the formation ofEM. This lack of storage would mostly appear in free recall tests rather than
1170
cued recall or recognition tasks (Christensen et al., 1998).
1171
Considerable data support the hypothesis that the weak EM performance of Alzheimer's patients might
1172
come from a deficit at the retrieval level of information, which appears to arise in the early stages of the disease
1173
(Perri et al., 2007) and leads affected individuals to forget quickly (Delis et al., 1991). AD patients typically have
1174
difficulties learning lists of words; moreover, once a list is learned, they quickly have difficulty recalling the
1175
words or recognizing them among distractors (Delis et al., 1991; Moulin et al., 2004; Traykov et al., 2007). As
1176
seen for encoding, patients benefit little from semantic cueing or environmental support, and their sensitivity to
1177
indicesdecreases as the disease progresses (Ergis and Eusop-Roussel, 2008; Libon et al., 1996; Wagner et al.,
1178
2012). They also appear to be unable to inhibit irrelevant associations (Helkala et al., 1989). However,
1179
contradictions appear:some studies have noted performance deficits for both recognition and free recall
1180
(Bäckman et al., 2001; Delis et al., 1991), while others found normal performance for recognition, at least during
1181
the first stage of the disease (e.g., Karlson et al., 2003; Tounsi et al., 1999). In some cases, free recall was found
1182
to be less successful in patients (e.g., Bartok et al., 1997; Kramer et al., 1988), and although the superior recall of
1183
pictures (compared to words) is preserved in AD patients (Ally et al., 2009), some authors found similar
31
1184
performances between recall and recognition tasks using both verbal and pictorial items (e.g., Deweer et al.,
1185
1993;Eslinger and Damasio, 1986; Fleischman et al., 1997; Grosse et al., 1990; Heindel et al.,1988; Koivisto et
1186
al., 1996;Greene et al., 1996). These findings suggest that the EM deficit observed among AD patients reflects
1187
an issue with learning rather than an acceleration of forgetting or disruption of retrieval. Tounsi et al. (1999)
1188
used the RL/RI 16 items test to examine 131 AD patients divided into four sub-groups according to the severity
1189
of dementia (i.e., pre-clinical to severe). Using a cued recall task, the authors showed that performance worsened
1190
withdisease progression, suggesting that retrieval is disordered at an early stage of AD. Retrieval deficits are also
1191
observed for autobiographical memory in patients with moderate stage of the disease, with consequences for
1192
future thinking. They are able to remember the past and imaging the future. However, patients will generate
1193
future events that are closely linked with their past memories, as few amount of memories are available (El haj et
1194
al., 2015a, 2015b). This inability to detach from the little information kept in memory to create new ones might,
1195
according to the authors, comes from a decline of flexibility, underpinned by the frontal lobes as well as from an
1196
alteration of the hippocampus.
1197
Piolino et al. (2003) demonstrated that familiarity processes are preserved in AD, whereasdeteriorations
1198
are seen in the controlled processes of conscious recollection. This conclusion is in line with the findings of
1199
Balota et al. (2002), who used a word recognition task in which they manipulated the frequency oftarget items
1200
and lures, and reported thatADpatients showed diminished performance on low-frequency words but not high-
1201
frequency words, as the latter triggered familiarity processes through their high frequency in the language.
1202
Conversely, lures were well rejected regardless of their degree of familiarity. Comparable results have been
1203
reported in MCI patients, with authors noting altered recollection but preservation of familiarity processes
1204
(Anderson et al., 2008; Hudon et al., 2009; Westerberg et al., 2006). Thus, it seems that recollection processes
1205
(i.e., those that allow subjects to retrieve items and their encoding context)may be sensitive right from the
1206
prodromal stage of AD,whereas familiarity processes are less sensitive. However, the deficits in encoding and
1207
consolidation increase as the pathology progresses,suggesting that rather thanbeing a sole deficit inretrieval, the
1208
desired information fails to be properly encoded.
1209
AD patients exhibit great difficulty in evoking memories and information, and also suffer from memory
1210
distortions (Balota et al., 2002; Budson et al., 2000; Dalla Barbaet al., 1999). Traditionally, studies in the field
1211
have focused on analyzing the negative symptoms that characterize the memory disorders related to Alzheimer's
1212
disease. More recently, however, researchers have turned to theso-called “positive” symptoms, such as extra-list
1213
intrusions, whichare the production of words that do not belong to the presented list in a recall task, and false
1214
recognition, which occurs when a subject is convinced that he or she recognizes an item even though it was not
1215
previously presented in the recognition task (Adam, 2006). Desgranges et al. (2002) suggested that different
1216
intrusions may arise via different processes: free recall intrusions that lack any semantic link to the target words
1217
may be attributed to deficits in strategic processes, reflecting a frontal dysfunction, whereas cued recall
1218
intrusions are induced relatively automatically by indices, reflecting rhinal dysfunction (Ergis and Eusop-
1219
Roussel, 2008). Several studies showed that ADpatients had a generally positive response bias (i.e., a tendency
1220
to always say “yes, I have seen this item”) in recognition tests (Pillon et al., 1993; Snodgrass andCorwin, 1988).
1221
Balota et al. (2002) used the mirror effect paradigm to account for this phenomenon. Subjects first memorize a
1222
series of words(50% with low lexical frequency, 50% high lexical frequency), and then are exposed to a
1223
distracting task before being testedwith a yes/no recognition task. The mirror effect paradigm predicts that low-
1224
frequency wordswill trigger more correct recognitions and less false recognition relative to items with a high
1225
lexical frequency. In AD, however, the opposite is observed. Budson et al. (2000), and Balota et al. (1999)
32
1226
showed that,compared to controls, Alzheimer's patientscommit fewer false recognitions after a single exposure
1227
to a list of semantically associated items, but show higher levels of false recognition after repeated exposure to
1228
the same list. This suggests that Alzheimer patients build up a semantic gist across trials, whereas controls
1229
distinguishacross all semantic items (i.e., if “tulip” is in list 1, “daisy” is in list 2 and “lily” is in list 3, controls
1230
will remember the semantic category of “flower” but not each individual item).
1231
6.3/ Neural structures implicated inEM declines
1232
The age-related decline in EMis a continuous process (Sexton, 2010) that arises from the dysfunction of an
1233
integrated network and (at least in AD) involves specific pathologies of both gray and white matter. Patients with
1234
a neurodegenerative disease, at least in the early stages of disease evolution, may present with very
1235
circumscribed neurocognitive impairment, as confirmed by the use of brain imaging. For example, Desgranges
1236
et al. (1998) used PET and a “cognitive-metabolic correlation” strategy to show that specific damages to
1237
different memory systems are related to specific and highly focused abnormalities in brain metabolism.However,
1238
impaired EM seems to be linked to dysfunction of an extensive network that includes the hippocampus and PFC
1239
(dorsal and ventral medial PFC, bilaterally), along with other regions, such as the posterior
1240
cingulate/retrosplenial cortex, the precuneus, the inferior parietal lobule and the hippocampal formation (i.e.
1241
entorhinal cortex and parahippocampal cortex) (Greicius et al., 2003; Laird et al., 2009). These structures are
1242
also known to be involved in the so-called default mode network(DMN; Eustache et al., 2006; Buckner et al.,
1243
2008 for reviews).The DMN, participating in EM (e.g. Shapira-Lichter et al., 2013), is an interconnected and
1244
anatomically defined brain system that preferentially activates in states of relative rest but deactivate during
1245
external-orienting tasks (e.g. Anticevic et al., 2012 ; Buckner et al., 2008). Deactivation of key nodes of the
1246
DMN, in coordination with hippocampal activation, may in fact be a prerequisite for successful memory
1247
encoding (Daselaar and Cabeza, 2004 ; Miller et al., 2008). Conversely, there is evidence that failure to suppress
1248
activity in some of the core default mode areas such as the precuneus is associated with failed encoding and poor
1249
performance in subsequent memory tests in cognitively normal young and old subjects (e.g. Otten and Rugg,
1250
2001)Several authors found a concordance between AD-related atrophy and healthy intrinsic functional
1251
connectivity in the DMN (Buckner et al., 2005; Greicius et al., 2004, Seeley et al., 2009).In recent fMRI studies
1252
of AD, corresponding brain default mode regions have been found to demonstrate an abnormal fMRI task-
1253
induced deactivation response pattern.Deactivation is progressively disrupted from normal aging to MCI and to
1254
clinical AD (Philajamaki and Sperling, 2009). In other words, the weaker the deactivations become in the DMN,
1255
the greater risk to develop the disease is important (e.g. Petrella et al., 2007). Moreover, the functionnal
1256
disconnection between the posterior cingulate cortex and the hippocampus may explain some of their EM
1257
impairments (e.g. Chételat et al., 2003 ; Villain et al., 2008).
1258
Most studies agree that the AD pathologybegins with the formation of NFT in the MTL. As the severity of
1259
the disease increases, the NFTprogressively accumulates and structural atrophy increases (Duyckaerts et al.,
1260
1998; Delacourte et al., 1999). In the early to moderate stages of AD, EM formation is critically underpinned by
1261
the hippocampal region (Baron et al., 2001; Desgranges, 2008) and the entorhinal cortex (Scheltens et al., 2002;
1262
for review, see Braak et al., 1999; Chételat and Baron, 2003; Taylor and Probst, 2008; see also Hirni et al.,
1263
2013). The temporo-parietal and posterior cingulate cortices are also affected, and the disease spreads to other
1264
neocortical regionsas the severity increases (Atienza et al., 2011; Gomez-Isla et al., 1996). In vivo imaging
1265
studies have shown that certain regions (e.g., the posterior parietal, cingulate and retrosplenial cortices) contain
33
1266
exceptionally high levels of amyloid plaques in AD patients, andamyloid deposition in the parietal cortex
1267
isnegatively correlated with glucose metabolism, suggesting that activity is diminished in this region (Klunk et
1268
al., 2004). As shown by Wolk et al. (2011), the neural substrates required to integrate and process information
1269
vary significantly depending on the stage of processing (i.e., encoding and/or retrieval).
1270
Functional disturbances of resting metabolism in AD brains have also been observed in a pattern
1271
mimicking structural modifications. A number of studies have reported either similar (Heun et al., 2007;
1272
Sandström et al., 2006) or increased MTL and notably increased hippocampal activity (Fleisher et al., 2005) in
1273
at-risk persons (i.e.,MCI patients orasymptomatic carriers of at least one ApoEɛ4 allele) compared to controls
1274
during EM tasks.However, hypometabolism and hypoperfusion of the temporo-parietal and posterior cingulate
1275
cortices constitute the earliest and most frequent dysfunction in AD(e.g.,Grön et al., 2004; Lind et al.,
1276
2006;Loessner et al. 1995) and are associated with pure EM disorders (e.g.,Desgranges and Eustache, 2005;
1277
Bäckman et al., 1999; Golby et al., 2005; Gron et al., 2002; Pariente et al., 2005). Asymmetry of the temporo-
1278
parietal cortex is reported in most PET studies of affected individuals with right hemispheric alterations noted in
1279
patients with MCI (Chételat et al., 2003; Mosconi et al., 2004) or moderate AD (Nagahama et al., 2003; for
1280
review, see Chételat et al., 2006). The reported results are somewhat heterogeneous, which can be explained in
1281
part by differences in the utilized methodologies and studied disease stages. For example, Desgranges et al.
1282
(2002) compared groups of patients at different stages of AD in an effort to follow the organization of brain
1283
networks during the course of the disease. EM was measured by PET analysis during retrieval, using a story
1284
recall test in a group of 40 patients divided into two subgroups (n=20 patients per group)based on their Mini
1285
Mental State Examination (MMSE) scores.For those having the highest MMSEscores (i.e. MCI), the significant
1286
correlationswere restricted to limbic structures, including the hippocampal, parahippocampal/perirhinal,
1287
entorhinal and retrosplenial cortices. This finding suggests that the dysfunction of these regions is responsible for
1288
the first declines in EM seen among AD patients. In the more severe subgroup, whichincluded patients with
1289
more profound pathology-associated memory deficits,correlations with EMwere found with regions of the
1290
neocortex, particularly the temporal lobe, which has been implicated in semantic memory. These correlations
1291
have been interpreted as reflecting a compensatory mechanism that is activated by the disease (for review, see
1292
Eustache et al., 2006). Compared to elderly controls, patients with mild AD show hypoactivations of MTL when
1293
encoding scenes or pictures (Machulda et al., 2003; Rombouts et al., 2000; Small et al., 1999), recognizing
1294
geometric patterns (Gron et al., 2002), and retrieving associations (Dickerson et al., 2005; Pariente et al., 2005;
1295
Sperling et al., 2003). In most studies, additional activations are seen in various neocortical regions, particularly
1296
the frontal (and also parietal) region, in patients with established AD (e.g.,Bäckman et al., 1999; Grady et al.,
1297
1993; Grossman et al., 2003; Rémy et al., 2005; Yetkin et al., 2006),and in MCI patients during EM tasks (Heun
1298
et al., 2007). During encoding and retrieval, patients showed consistently greater activity in the right DL-PFC
1299
and left or bilateral VL-PFC when compared to controls. The observed PFC differences between patients and
1300
elderly controls were unidirectional, with AD patients showing greater PFC activity than controls. A relationship
1301
between VL-PFC and the MTL has been documented, in that the degree of activity in the left VL-PFC is greater
1302
in older adults with less MTL activity during encoding (Gutchess et al., 2005). The same phenomenon has been
1303
observed in the medial parietal cortex and posterior cingulate gyrus(Sperling et al., 2003, Fouquet et al.,
1304
2007).Although overactivation might support improved performance in the short term, it could also be a sign that
1305
an individual is compensating for a progressive pathology (and therefore could predict future declines).
1306
In recent years there has been an emphasis in exploring the dynamic properties of the subregions (dentate
1307
gyrus, Ammon’s horn, subiculum) of the hippocampus rather than examining the hippocampus as a
34
1308
homogeneous structure. Indeed, subfields of the hippocampus are not uniformly affected by the disease. The
1309
function of the dentate gyrus (DG) is manifold but it has a key role in the processing of spatial information and
1310
memory processes : formation of new memories (Zhao et al., 2008), associative memory (Morris, 2006), spatial
1311
pattern separation (Kesner, 2013), context pattern separation (Lee and Solivan, 2010 ; Wei Deng et al., 2013) for
1312
some of its main role. The human dentate gyrus have the unique property of persistent adult neurogenesis (Li et
1313
al., 2008). It is thought to play an important role in hippocampus-dependent learning and memory. Li and
1314
colleagues found that, in AD, although neuroproliferation increase, the differentiation of newly born cells into
1315
mature neurons is compromised. However, the dentate gyrus has been shown to withstands neurodegenerative
1316
disease markers until late stage of AD (Ohm, 2007). This is also true for the CA3 region, part of the ammon’s
1317
horn (Gómez-Isla et al.,1996). On the contrary, the CA1 zone is vulnerable to the disease as an atrophy, neuronal
1318
loss and NFT are observed (Mueller et al., 2010 ; Pluta et al., 2012, West, 1994). The anatomy suggests that the
1319
subiculum might participate in multiple reverberating circuits linking the hippocampus and the wider temporal
1320
cortex. It would compare novel stimuli from the entorhinal cortex with temporarily stored information in the
1321
hippocampus (Witter et al., 2000). The subiculum might also receive multiple mapped versions of the same
1322
space possibly facilitating the construction of distinct spatial maps (Menendez, 2006). Although mildly affected
1323
in early stages, significant reductions in the amount of dendrites (i.e. neural number) have been shown in AD,
1324
particularly in later stages (Rossler et al., 2002 ; West, 1994).
1325
Finally, although the cerebellum is not considered to be a primary focus of AD pathology, differences have
1326
been noted in cerebellar regions upon both encoding and retrieval. Indeed, while the cerebellum was traditionally
1327
thought to be unaffected in AD, neuropathological studies haveidentified cerebellar changes in the late stage of
1328
the disease (Rapoport et al., 2000; Wegiel et al., 1998). One study revealed that patients showed very large
1329
activationsof the left and right cerebellar hemispheres upon encoding (however, this work failed to specify the
1330
disease stage)(Schwindt and Black, 2009). Ishii et al. (1997) found that cerebellar metabolism was decreased in
1331
severe AD, and this decrease was correlated with the MMSE score. Together, these results suggest that atrophy
1332
progresses with the severity of AD, spreading from the MTL to the entire cortex.
1333
In sum, EM impairment is reached very early in AD patients and differ according to the severity of the
1334
disease. These performance deficits reflect specific disorders to one or more of the steps of encoding, storage
1335
and/or recovery, but also the creation of false memories, such as the production of intrusion and false
1336
recognition.The pattern of EM impairments displayed by AD patients is consistent with damage to areas of the
1337
MTL (the entorhinal cortex being affected first) and frontal lobes. MRI findings have also suggested that the
1338
fornix and mammillary bodies are atrophied in AD compared with healthy controls and with patients with MCI.
35
1339
7/ Conclusion and perspectives
1340
Over the last few years, neuroimaging studies (fMRI and PET) conducted on EMhave revealed that
1341
different brain networks are involved in healthy elderly subjects or AD patients compared to the reference
1342
population (i.e., young subjects). However, the study of EM has not been limited to PET- and fMRI-based
1343
methodologies,and numerous researchers have used other techniques, such asevent-related potentials(ERPs) or
1344
transcranial magnetic stimulation(TMS), to explore the responses of thebrain. The age-related decline in EM has
1345
been associated with structural and functional alterations in the PFC, the MTL (including the hippocampus and
1346
parahippocampal regions), the parietal lobe, the cingulate gyrus, and the cerebellum. Such studies have further
1347
suggested that different mechanisms may be involved in age-related versus pathology-related memory
1348
impairments.
1349
In normal aging, changes in the PFC (the most sensitive structure) seem to underlie the age-related
1350
declines in memory performance, at least among the oldest subjects. The central role of this structure is also
1351
emphasized by the finding that its activity increases in response to the under-recruitment of the MTL, reflecting
1352
a compensatory mechanism (for an example, see Gutchess et al., 2005). EM difficulties also appear to be linked
1353
to more general declines in attentional, executive and speed processing, which are further associated with
1354
volume reductions in the frontal cortex. From a behavioral point of view, Craik and Jennings (1992) noted that
1355
age effects are difficult to characterize in terms of a single dimension, instead appearing to represent a complex
1356
interaction between participants, materials, and variables of encoding and retrieval. The existence of a cognitive
1357
reserve, although difficult to measure, could also explain the apparent discrepancies between the results of
1358
different studies.
1359
Understanding the age-associated deficits in memory is important for two reasons. First, in view of the
1360
growing number of older adults in today’s society, cognitive aging is increasingly becoming a problem of
1361
general health care, and effective therapeutic intervention methods can only be developed on the basis of
1362
knowledge obtained through fundamental research. Second, there is a subgroup of elderly with more severe
1363
memory impairments that prevent them from functioning normally within their environment. Such memory
1364
impairments can be the earliest manifestation of pathological age-related conditions, such as AD. Particularly in
1365
the early stages of the disease, it is difficult to distinguish the AD pathology (i.e., EM impairments) from normal
1366
age-related memory impairments. In the first stages of the disease (i.e., MCI), the entorhinal cortex and its
1367
associated structures in the anterior MTL are affected (Hirni et al., 2013). The AD lesions progress to the parietal
1368
cortex and neocortex,and then affect the frontal lobe. Thus, the brain areas that sub-serve residual EM shift from
1369
the limbic to the neocortical structures as the AD-related cognitive impairment becomes more severe. Deficits in
1370
EM are already present in patients with MCI, potentiallyreflecting the first symptoms of disease.Thus, even if
1371
activities of daily living are preserved, EM impairments could constitute an important early marker that
1372
neurologists might use to identify individuals at higher risk for developing AD.
1373
Going forward, the challenge will be to further advance our understanding of the biological and
1374
psychological aspects of memory in normal aging, such that specific lifestyle changes (e.g., an exercise regimen
1375
and dietary supplements) and pharmacological treatments can be recommended to middle-aged and older adults,
1376
in the hopes of supporting satisfactory memory performance and relatively independent living well into the ninth
1377
and tenth decades of life. Successful treatments would presumably be those that increase the recruitment of
36
1378
additional neural networks to support declining networks whose functions have become inefficient and/or noisy.
1379
This may arise through the multiple mechanisms of neural plasticity that continue to function in older adulthood.
1380
37
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Figure 2: The three processes of episodic memory and their neural substrates. Abbreviations: MTL, medial
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temporal lobe; and mPFC, medial and lateral prefrontal cortices.
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Figure 3: Progression of Alzheimer’s disease (AD) according to the amount of cognitive reserve (CR; high or
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low). The stars indicate the critical threshold of brain damage, beyond which the clinical signs of AD are seen
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(Hall et al., 2007).
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S1568-1637(15)30019-2 http://dx.doi.org/doi:10.1016/j.arr.2015.08.006 ARR 604
To appear in:
Ageing Research Reviews
Received date: Accepted date:
23-6-2015 20-8-2015
Please cite this article as: Tromp, D, Bernard, F, Dufour, A, Lithfous, S, Pebayle, T, Despr´es, O, Episodic memory in normal aging and Alzheimer Disease: Insights from imaging and behavioral studies.Ageing Research Reviews http://dx.doi.org/10.1016/j.arr.2015.08.006 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.
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Episodic memory in normal aging and Alzheimer Disease:
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Insights from imaging and behavioral studies
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Tromp Da, Bernard Fa,Dufour Aa,b, Lithfous Sa, Pebayle Tb and Després Oa
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a: Laboratoire de Neurosciences Cognitives et Adaptatives (LNCA - UMR 7364 - CNRS/UDS) - 21 rue
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Becquerel, 67087, Strasbourg. France - [email protected]
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b: Centre d'Investigations Neurocognitives et Neurophysiologiques (CI2N - UMS 3489 - CNRS/UDS) - 21
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rue Becquerel, 67087, Strasbourg. France
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Corresponding author:
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TROMP Delphine
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21 rue Becquerel
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67087 Strasbourg Cedex
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FRANCE
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Tel: +33 (0)3 88 10 67 66
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Fax: +33 (0) 388.106.245
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E-mail: [email protected]
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1/ Introduction .................................................................................................................................................. 5
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2/ Episodic memory processes and cerebral substrates ....................................................................................... 7
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2.1/ Encoding ............................................................................................................................................... 8
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2.2/ Consolidation or storage......................................................................................................................... 9
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2.3/ Retrieval .............................................................................................................................................. 10
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3/ Behavioral data and models clarifying the memory decline performance in normal aging ............................. 12
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4/ Chemical and anatomical data: role of brain imaging study in healthy elderly .............................................. 15
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4.1/ Depletion of neurotransmitters ............................................................................................................. 15
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4.2/ Prefrontal cortex .................................................................................................................................. 17
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4.3/ From HERA to HAROLD: the compensation models ........................................................................... 17
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4.4/ Aging in the PFC: link with behavioral data ......................................................................................... 20
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4.5/ Medial temporal lobes .......................................................................................................................... 21
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4.6/ Are other neural substrates of EM affected by age? ............................................................................... 24
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5/ Inter-individual variability associated with EM in normal aging and Alzheimer disease................................ 26
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5.1/ Lifestyle .............................................................................................................................................. 26
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5.2/ Genetics............................................................................................................................................... 27
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6/ Episodic memory and Alzheimer disease ..................................................................................................... 30
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6.1/ Pathophysiology and characteristics of the disease ................................................................................ 30
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6.2/ Behavioral data .................................................................................................................................... 31
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6.3/ Neural structures implicated in EM declines ......................................................................................... 33
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7/ Conclusion and perspectives........................................................................................................................ 36
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Highlights
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Episodic memory is sensitive to the effects of age and very disrupted in Alzheimer’s disease. It is the first memory system to decline in both normal and pathological aging.
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Neuroimaging studies have been fundamental in distinguishing between normal aging and AD: they
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have shown a particular pattern of morphological and functional distinct brain damage. The prefrontal
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cortex seems to be affected first in non-demented adults whereas the hippocampus is the primary
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structural disorder in this neurological disease.
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Interindividualvariabilities observed during episodic memory performances could be due to several factors including lifestyle and genetic factors.
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Additional or different neurocognitive processes seem to develop both in normal and pathological brains to offset the deficit of episodic memory.
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Abstract
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Age-related cognitive changes often include difficulties in retrieving memories, particularly those that rely on
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personal experiences within their temporal and spatial contexts (i.e., episodic memories).This decline mayvary
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depending on the studied phase (i.e., encoding, storage or retrieval), according to inter-individual differences,
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and whether we are talking about normal or pathological (e.g., Alzheimer disease; AD) aging. Such cognitive
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changesare associated with different structural and functional alterations in the human neural network
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thatunderpins episodic memory. The prefrontal cortex is the first structure to be affected by age, followed by the
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medial temporal lobe (MTL), the parietal cortex and the cerebellum. In AD, however, the modifications occur
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mainly in the MTL (hippocampus and adjacent structures) before spreading to the neocortex. In this review, we
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will present results that attempt to characterize normal and pathological cognitive aging at multiple levels by
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integrating structural, behavioral, inter-individual and neuroimaging measures of episodic memory.
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Keywords: Episodic memory, fMRI, PET, Normal aging, Alzheimer disease
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1/ Introduction
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According to Eurostat (the European Statistical Institute),the proportion of people over 65 years old will
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increase until 2060, when it will reaching 30% of the European population (compared to 16% in 2010). At this
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same time, people over 80 years are predicted to represent 12% of the population (compared to 5% in 2010).
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According to the European Commission’s 2009 Ageing Report, the number of European persons older than 65
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years suffering from at least one disability in activities of daily living will more than double between 2007 and
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2060, reaching 44.4 million by the latter date.This consistent increase inthe aging population will come with
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important health and economic stakes (Freund and Smeeding, 2010; Lutz et al., 2008). We will be challenged to
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allow this aging to occurunder the best possible conditions, and this will need to ‘create a substantial financial
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burden. In 2010, expenses related to the frail elderly (seniors who have lost autonomy) in France were estimated
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to be between 27 and 34 billion euros.
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Normal aging generally induces cognitive impairment, with older people often considered to be less
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efficient than younger people in using memory, attention, visuospatial capacities or executive functions. While
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most aging individuals experience some degree of “normal” cognitive change, the incidence of the
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neurodegenerative diseases collectively classified as “dementia” also increases dramatically with age.Among
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them, alzheimer disease (AD) constitutes the leading cause of dementia in persons aged over 60 years, reaching
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6.7% in subjects 75-79 years old and 31.15% in those over 85 years old (Helmer et al., 2006).
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One of the earliest cognitive changes in aging, and the one that has probably received the most
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attention, is the alteration of memory (Grady, 2008; Park and Gutchess, 2002). Older people exhibit changes in
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the quality of their memories (Friedman et al., 2010; Piolino et al., 2006; Schacter et al., 1997), in
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associationwith difficulties in remembering (Craik and Bialystok, 2006; Davis et al., 2003; Ozen and Rezaki,
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2007). Memory changes are also the most striking cognitive alterations seen in pathological aging, butmemory
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loss in normal aging qualitatively differs from that associated with a diagnosis of AD (for review, see Budson
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and Price, 2005). Major research efforts have focused on trying to distinguish the memory declines attributable
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to normal aging from those that indicate pathological aging, particularly AD(e.g. Ghosh et al., 2011). Such
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studies have shown that we do not have unitary memory; rather, both cross-sectional and longitudinal studies
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have demonstrated that the different memory component systems do not age uniformly, but instead show
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differential vulnerabilities to the effects of aging (Brickman and Stern, 2009).
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The long-term memory (LTM) system is divided into two broad classes: explicit (declarative) memory,
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which requires the conscious recall of information, and implicit (non-declarative) memory, which is based on
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implicit learning (Squire, 1987). Implicit memory includes procedural memory and the Perceptual
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Representation System (PRS),sustainingpriming effects and operant or classical conditioning. In contrast,
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declarative memory is subdivided into semantic memory and episodic memory (EM). Semantic memoryis
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related to general facts and knowledge,whereas EM is a cognitive system that enables an individual to record (or
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encode), store, and retrieve information about personal experiences and the temporal and spatial contexts of
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those experiences (first defined by Tulving, 1972). The classic model of EM refers to both the autobiographical
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recollection of one’s personal past experiences (e.g., What did you eat for breakfast this morning?) and
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laboratory tasks requiring the conscious recognition or recall of experimental materials (e.g., a list of words).
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Although autobiographical memory (AM) has often been equated with EM, it is important to distinguish
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between the two. AM may encompass long periods and is defined by self-related information processing,
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subjective emotional evaluation of memories and a quick, intuitive and pre-conscious feeling of certainty (a
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“feeling of rightness”)to control the veracity and cohesiveness of retrieved memories (Cabeza and St. Jacques,
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2007; Gilboa, 2004; Moscovitch and Winocur, 2002).This memory system consists of episodes recollected from
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an individual’s life based on the combination of episodic (also called episodic autobiographical memory) and
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personal semantic memory (semantic autobiographical memory). In other words, it includes both one’s self-
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knowledgeand the memories that surround this self-knowledge (e.g. Abram et al., 2014; Markowitsch and
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Staniloiu, 2011; Martinelli et al., 2013).Experimental memory, in contrast, is measured in seconds, minutes and
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hours; it is rare and only really considered in cases of psychological and laboratory experiments. Wheeler et al.
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(1997) proposed that,unlike AM, EM requires elaborate, conscious monitoring and awareness to avoid omissions
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and repetitions, and also involvesthe intentional use of retrieval strategies. As AM and its age-related declines
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have already been the subject of many studies and reviews (e.g. Piolino, 2003), the present review will only
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address experimental episodic memory (referred to as EM hereafter).
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The above-described types of memory are all part of the LTM system, where information can remain
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for an infinite time(Glisky, 2007). In contrast, working memory (WM) refers to the active storage and cognitive
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manipulation of information necessary for complex cognitive tasks, in order to achieve an immediate goal (e.g.,
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remembering a phone number). WM is a subcomponent of short-term memory (STM), whichis known to involve
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the passive maintenance of information in the mind over a short period(Cowan, 2008). A classification of the
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different memory systems is presented in Figure 1.
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Aging affects the various memory systems to different degrees, and numerous inter-individual
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differences are seen. While some older adults have significant cognitive deficits, others maintain performances
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equal to those of younger individuals(e.g. Angel et al., 2010; Butler et al., 2004; Shimamura et al., 1995). Some
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systems, such as short-term and procedural memory, do not seem to be affected by normal aging (Brickman and
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Stern, 2009; Craik, 1977; Nilsson, 2003; Zacks et al., 2000). Semantic memory also appears to be immune to
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some of the effects of aging, in that general knowledge and vocabulary are well maintained in older adults (e.g.
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Verhaeghen, 2003; Kennedy et al., 2015).In contrast, EM is highly affected by aging (e.g. Balota et al., 2000;
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Luo and Craig, 2008; McDaniel et al. 2008). This is likely to reflect that EM depends on many processes that are
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underlain by a vast cerebral network. The frontal system, which gives EM a certain consistency by organizing
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information, acts in parallel with the temporal hippocampal system in controlling and organizing the encoding
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and retrieval of EM information via the selection, initiation, elaboration and implementation of relevant
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strategies (Kraemer et al., 2005).Other (far less well studied) structuresare also involved, such as the parietal
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cortex and the cerebellum (the best studied among them), as well as the thalamus and the cingulate gyrus (Wiggs
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et al., 1999; for review, see Cabeza and Nyberg, 2000).Changes at the neuroanatomical, neurophysiological and
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neurochemical levels of the central nervous system are likely to underpin the observed age-related decline in
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EM: decrease in white and gray matters volumes, neuronal numbers and size, reduced efficiency of synaptic
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contacts and decreases in the concentrations of neurotransmitters (Raz, 2000; Burke and Barnes, 2006; Deenis
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and Cabeza, 2008 for a review).All of these changes preferentially affect the frontal brain regions (for review,
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see West, 1996). Post mortem (Meltzer et al., 2003) and in vivo studies haveshown that, compared to the brains
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of young adults, the brains of older adults tend to have lower volumes of gray matter according to an antero-
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posterior gradient (Resnik et al., 2003). Cross-sectional studies suggest that the gray matter volume declines
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steadily across the adult lifespan, whereas the white matter volume increases linearly from birth to young
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adulthood, plateaus during middle age, and declines during old age (Raz et al., 2005). In vivo volumetric studies
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of healthy volunteers have revealed the presence of a significant hippocampal shrinkage (up to 1.18% per year)in
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people in their mid-50s (Lemaître et al., 2005; Raz et al., 2004; Resnick et al., 2000; see also Fjell et al., 2009),
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and to an early and severe atrophy of the prefrontal cortex (PFC) after the age of 20, with an estimated average
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decline of about 5% per decade (Raz and Rodrigue, 2006). On a larger scale, this selective PFC decline observed
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in the elderly (particularly in the dorsolateral PFC; Kraemer et al., 2005) is associated with degradation of the
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executive functions (Allain et al., 2007; Raz, 2000; Shallice, 1982; West, 1996), which are a heterogeneous set
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of high-level cognitive processes that allow the subject to show flexible behavior and adapt to new
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situations(e.g., anticipation, planning, monitoring and control of action; problem solving; task flexibility;
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selection of relevant information; inhibition of automatic responses; and the exclusion of information that
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isirrelevant for the execution of a given task).All of these functions are involved in both encoding and retrieving
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information (Benton, 1994; Isingrini and Taconnat, 2008). Research in this area has repeatedly shown that
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alterations in the PFC negatively impact the functioning of memory, especially in its strategic aspects; EM
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deficits are also likely to reflect the degradation of certain cognitive resources, such as speed processing,
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inhibitory functions and attentional resources(e.g., Glisky, 2007; Groth and Allen, 2000; Wascher et al., 2012).
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The first data regarding cognitive aging, particularlychanges in EM, were collected from studies of
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brain-damaged patients (Wheeler et al., 1995; for review, see Werkle-Bergner et al., 2006)and experimentally
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lesioned animals (Aggleton and Brown, 1999; Miller and Cohen,2001). More recently, functional neuroimaging
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techniques, such as functional Magnetic Resonance Imaging (fMRI) and Positron Emission Tomography (PET),
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have been used to determine the brain modifications related to this decline. Meanwhile, cognitive aging studies
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have described the effects of aging on behavioral performance, and neurobiological studies have characterized
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the effects of aging on the brain. Then, in vivo neuroimaging techniques have been used to bridge the gap
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between these two techniques, allowing researchers to characterize the brain in action and examinethe neural
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substrates of cognitive aging that link behavior and function.The present paper aims to review neuroimaging
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results, especially fMRI and PET studies, andexplore the functional and cerebral activations associated with EM
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and behavioral disorders in the healthy elderly and patients with Alzheimer-type dementia.
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- Insert Figure 1 about here –
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2/ Episodic memory processes and cerebral substrates
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A major feature of the EM system, unlike other systems of LTM facing the present,is the ability to be
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aware of personal memories. This arises via“mental time travel” (Tulving, 2002), which is our ability to relieve
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past experiences and project ourselves into the future. EM is fundamental to the individual, as memories of
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personal experiences form the basis for the construction of identity. This memory can be tested verbally or non-
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verbally.During an episodic retrieval task,an individual is usually able to associate an EM (e.g. a word from a
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list) with particular details, such as the relevantemotion, time, place, and other particulars. The quality of
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memory storage depends on the processes involved in the encoding, storage and recovery of information (Figure
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2).
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2.1/ Encoding
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Encoding operates through the transformation of information that comes from external stimuli (e.g.,
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perceptual and sensory details, personal information, or spatial and temporal details) or triggers cognitive
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processes, and integrates the data in the form of a mental representation. Various sources are generally used to
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test experimental EM encoding; these can include verbal material (words), non-verbal material (pictures, scenes,
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objects, music, etc.), andthe context (i.e., source memory), the latter of which refers to the conditions
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surrounding the encoding of a particular episodic memory and the features under which it was acquired (Johnson
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et al., 1993). The context can serve as an indication for future recovery, asthe recollection of contextual details
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can allow an individual to distinguish a specific event from other similar events. During tests of contextual
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memoryparticipants are asked about the source of the experience (e.g.,Did person A or B report the event?), and
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various contextual details, including the color (e.g., Guo et al., 2013), vocal (e.g., Glisky et al., 2001), visual
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(e.g.,Fernandes and Manios, 2012), spatial (Cansino et al., 2015), and emotional (e.g., Bo and Xiao-Lan, 2012)
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context in which a word or event was presented. All of these details contribute to making EM multimodal,
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contextual, associative, and unique. Encoding is the first stage of memory, and it is crucial for the storage and
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retrieval ofvoluntary stored information. Many authors have described the processes of EM within a
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constructivist design (e.g., Schacter et al., 1998). During learning, the brain must form a neural representation of
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the new experience. A personally experienced episode is represented as a pattern of features that correspond to
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the different facets processed during the encoding of the episode(Gottlieb et al., 2012). These features are widely
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distributed in the brain, such that no single location contains a complete record of the memory trace of a specific
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episode(Squire, 1992). Multiple sensory structuresprocess the different stimuli and information regarding the
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identity of perceptualobjects and events. For example, the visual cortex is responsible for recognizing faces,
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letters, and the colors of letters, while the olfactory and auditory cortices recognize other facets of an experience.
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The neuronal activities arising from these cortices converge into the medial temporal lobe (MTL), where the
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perirhinal cortex, the lateral entorhinal area, the parahippocampal cortex and the medial entorhinal cortex treat
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the information.The inputs then converge at the hippocampus to become cohesive memories of individual events
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via the formation (“binding”)of EM (Kessels et al., 2007; Lekeu et al., 2002; Piolino et al., 2010). When such
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binding is faulty or absent, the individual may recover only fragments of the episode, not the whole pattern
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(Clayton et al., 2003). After binding, the outputs of the hippocampusreturn to the cortical areas from which the
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inputs arose (i.e., the perirhinal–lateral entorhinal cortex and parahippocampal–medial entorhinal
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cortex).However, information reaches the hippocampus every second of every day.The amygdala filters
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memories by evaluating their emotional content: if this latter is strong, this part of the brain informs the
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hippocampus to enhance storage of the event (e.g. Phelps, 2004).When an individual recalls a memory, the
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printed neural map in the hippocampus is reactivated, mobilizing the brain regions that were involved in forming
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the memory (i.e., the visual, olfactory and auditory cortices). This was shown by Wheeler et al. (2000), who
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reported that the sensory regions specifically activated during the encoding of images (occipital cortex) or
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sounds (temporal cortex) were reactivated when these memories were recalled. In parallel,a dialog between the
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hippocampus and the PFC allows the memory to re-emerge into consciousness (Preston and Eichenbaum, 2013).
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The type of information processing that occurs during the encoding stage determines the quality of both
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the encoding and the recovery of that information. Before the emergence of the neuroimaging techniques
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thatallow researchers to study the neuroanatomical bases of the encoding process, this process was primarily
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studied by manipulating the nature of the stimuli (verbal, pictorial), the sensory modality (auditory, visual), the
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time of presentation, and the way in which the studied individuals implemented strategies to better learn and
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remember information (e.g., mental rehearsal, phonological association, and organization of the material, such as
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through the construction of sentences or semantic categorization)(Gershberg and Shimamura, 1995; Turner et al.,
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2007).According to the treatment level design proposed by Craik and Lockhart in 1972, “the persistence of the
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memory trace is a function of the depth of treatment, levels of deep treatment being associated with more
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elaborate memory traces stronger in time, and more robust.”Indeed, the deeper the treatment, the stronger and
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lasting the memory trace. Superficial encoding simply relies on the structure of the stimulus (e.g. the number of
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vowels in a word), whereas deep encoding (e.g. the production of mental images) gives meaning to the stimulus,
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explores its relationship with other objects or situations, and thus has a positive impact on the memory trace(see
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Galli, 2014 for review).
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The relevant studies typically fall into two groups: intentional and incidental encoding studies. During
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the former, participants are scanned while attempting to memorize words, faces, objects, or spatial routes.
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During incidental encoding, in contrast, participants are usually asked to make a judgment concerning the stimuli
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presented during encoding (i.e., regarding semantics or size), without any attempt at memorization. To assess the
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neural bases of EM encoding using fMRI or evoked potentials, many authors have used the subsequent memory
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paradigm (also referred to as the “difference due to memory” or “Dm” paradigm) (Sanquist et al. 1980). In this
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paradigm, participants encode stimuli either intentionally or incidentally during scanning, and theneural activity
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associated with successful encoding of items that are subsequently remembered in a recognition test is compared
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to that observed during the encoding of items that are subsequently forgotten (Brewer et al., 1998; Wagner et
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al.,1998; for review, see Paller and Wagner, 2002). Several neuroimaging studies have shown, for example, that
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when neural activity supports successful encoding,thefMRI signal is greater for stimuli that are subsequently
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remembered compared to those that are forgotten (e.g. Bernard et al., 2004; Duverne et al., 2009; Kim, 2011).
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According to some studies, the encoding process seems to be disturbed by aging, with encoding
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deficiencies predominating over retrieval deficits in older adults (e.g. Friedman et al., 2007; Morcom et al.,
281
2003). Nevertheless, encoding maintains a strong link with retrieval, and it is very difficult to separate the effects
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of encoding from those of retrieval in behavioral studies. This especially true given that retrieval tasks are used
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to measure memory performance,the success of retrieval depends on the success of encoding, andsome theories
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favor an overlap between these two processes.Most of the research on encoding has been conducted in rather
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young or rather old adults, with the younger adults usedas the reference group for comparison. This makes sense
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given that younger adults usually encode with much higher accuracy (Miller, 2013). Age-related declines in
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source memory are considered to be important for explaining the age-related deficits in EM. In
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addition,features(i.e. physical, visual, olfactory…) are less well remembered by older adults compared to
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younger adults, with older individuals showing poorer memory for the perceptual features of auditory inputs,
290
such as a speaker’s voice (e.g. Bayen and Murnane, 1996).
291
2.2/ Consolidation or storage
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After the encoding phase, a process of information consolidation is initiated, allowing performance to
293
be maintained andreorganized into LTM.Two models of consolidation exist: the Standard Model (SM) of
294
memory consolidation and the Multiple Memory Trace (MTT) (Nadel et al., 2007). First described by Scoville
295
and Milner (1957), the SM theory stipulates that memory storage initially requires the hippocampus to linkthe
296
different features of the memory, which are dispersed across numerous sites in the neocortex (Alvarez and
9
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Squire, 1994; Dudai, 2004; Squire and Alvarez, 1995). Over time, however, the requirement for the
298
hippocampus dissipates (Meeter and Murre, 2004) and the representation of the memory becomes solely
299
dependent on the neocortical storage sites (Frankland and Bontempi, 2005). This change in function over time is
300
believed to account for the retrograde amnesia gradients often seen in patients with hippocampal damage. In
301
contrast, the MTT theory posits that all memory traces incorporated since birth are combined into a multiple-
302
trace representation in the brain. In this model, the hippocampus and neocortex continue to interact with each
303
other during EM,forming the memory trace of an episode (Nadel and Moscovitch, 1997 for a review; Nadel et
304
al., 2000). Contrary to the SM theory, the concept of MTTassumes that the MTL has no longer a temporary role
305
in the storage and retrieval of memory but a permanent one. The hippocampus is always involved whenever
306
detailed, contextual information is recalled (Hoscheidt et al., 2010; Piolino et al., 2008; Winocur et al., 2010;
307
Figure 2). However, semantic information of the memory, which has no contextual richness and would then be
308
more a schematic version of the memory, seems to be established in the neocortex alone(Harand et al.,
309
2012;Nadel et Moscovitch, 1997).Episodic memories consolidation is measured by delayed recall in time of the
310
previously recorded information (encoding) and after an interfering activity.However, this recall will only be
311
useful if theimmediate free recall is correct (see below), insofar as only properly encoded information can be
312
consolidated. Sleep is an important step in the consolidation of memory (e.g.Walker andStickgold, 2006), as the
313
neural sequences involved in daytime learning are reactivated during the deep sleep and REM (Rapid Eye
314
Movement)sleep phases (e.g. Rauchs et al., 2010). The effect of sleep on memory consolidation in aging has
315
only been sparsely studied, and appears to be characterized by wide inter-subject variability in the elderly
316
(Dudai, 2004; McGaugh, 2000; see also Alberini and Leroux, 2014).Therefore, we will only mention it briefly
317
here.
318
2.3/ Retrieval
319
Unlike short-term memory, LTMrequires the retrieval of information that is no longer being maintained
320
in an active state. Retrieval processes are required to reactivate its mental representations and return the
321
individual to his or her conscious experience of the event (Tulving, 1983).The aging process strongly affects
322
retrieval, but the importanceof such age-related differences may differ depending on the task used to assess EM
323
performance (e.g., free recall, cued recall or recognition)(for reviews, see Balota et al., 2000; Brett et al., 2012;
324
Craik and Jennings, 1992; Light, 1991; Luo and Craik, 2008; McDaniel et al., 2008; Zacks et al., 2000). In free
325
recall (Arnold andMcDermott, 2013), a person is given a list of items to remember during encoding (e.g., words,
326
sounds or pictures) and is then tested by being asked to recall as many items as possible in any order following a
327
delay of variable duration. The experimenter notes the number of items correctly recalled as well as the number
328
of intrusions (words that were not studied but are mistakenly recalled), which is more likely in AD patients than
329
in normal controls (Dalla Barba and Wong, 1995).
330
In cued recall, a person is given a list of items to remember during encoding and is then tested with cues
331
aimed at helping them remember the material, such as the shape of the first two or three letters of an encoded
332
word, or the first word of a pair ofencoded words.
333
Recognitionrefers to an individual’s ability to judge whether an event or item had been
334
previously“lived” or “seen”.Participants study a list of stimuli, and are then scanned while being given an old–
335
new recognition test in which they are asked to judge whether they recognize the item as “old” (seen during the
336
study phase) or “new” (Besson et al., 2013 for a review). Within the settings of either an event-related fMRI
10
337
paradigm or event-related potentials, the neural activity associated with correct “old” responses (hits) is
338
contrasted with the activity associated with correct “new” responses (correct rejections). Two other basic
339
categories of recognition memory errors are often encountered during memory tests: false alarms (i.e., false
340
recognitions) and misses(i.e., the failure to identify a previous occurrence as old) (Schacter et al., 1997). These
341
memorydistortions (or false memories) occur when a remembered event either never occurred or the memory
342
differs substantially from reality.False memories can be experimentally induced by usingtheDeese-Roediger-
343
McDermott (DRM) paradigm, (Roediger and McDermott,1995).
344
In recent years, the measures of EMin recognition studies have evolved to take into account two
345
essential components: responses that depend on controlled retrieval (“recollection”) and those that rely on a
346
simple judgment of familiarity. Recollection is defined as “the mental reinstatement ofa previous event”
347
(Skinner and Fernandes, 2007). Details of a memory are recalled, such as the sounds associated with an event,
348
the emotions felt during the first presentation of the item or event, and/or the mental state of the subject being
349
tested. Familiarity, in turn, refers to the subject’s being able to sense that an event (or an item) has been
350
experienced in the past, but being unable to recall any detail. Thus, it is possible to achieve some memory tasks
351
when the recall is impaired and but the familiarity (or lack thereof) is not. The form of consciousness associated
352
with the memory also distinguishes these two forms of response, with autonoetic consciousness associated with
353
EM for recollection, andnoetic consciousness involving internal representations and linked to semantic memory
354
for familiarity(Gardiner and Richarson-Klavehn, 2000). Using the Remember/Know paradigm (R/K; Tulving,
355
1985), it is now classical to separately evaluate these two forms of information accessusing an introspective
356
approach that aims to assess the state of consciousness that accompanies recognition.For each item classified as
357
“old” on a recognition test, participants are asked to indicate whether their memory is vivid and rich in
358
contextual detail (“Remember”): whether the item was written in color, as well as whether upper- or lowercase
359
was used, whether they can describe the experimenter’s voice, whether the task was auditory,or whether the
360
participant classified it as “old” based on a non-specific sense of familiarity rather than a vivid memory
361
(“Know”) (Gardiner, 1988; Gardiner and Java, 1993; Yonelinas, 2002, see Migo et al., 2012 for a review). If the
362
participant seems to have trouble making a decision, he or she may be questioned regarding thedegree of
363
certainty (for review, see Gardiner et al., 2002). Another approach involves analyzing confidence judgments
364
with the Receiving Operator Characteristics (ROC) method (Yonelinas, 2001). During the recognition task,
365
participants must judge whether they have a high or low degree of confidence that theysawa given item during
366
the encoding task, or if they think the item was not previously presented.
367
In their review focusing on the brain networks underlying episodic memory retrieval, Rugg and Vilberg
368
(2013) stated that the recollection of information isassociated with the engagement of a neural network that is
369
centered on the MTL and includes the hippocampus, parahippocampus, and perirhinal cortices. Together, they
370
are interconnected with cortical regions (e.g., theretrosplenial and posterior cingulate cortex, the angular gyrus,
371
and the medial and lateral prefrontal cortex; mPFC)to retrieve past events(Figure 2).
372 373 374
-Insert Figure 2 about here -
375 376
11
377
3/ Behavioral data and models clarifying the memory decline performance in normal aging
378
EM performance gradually deteriorates from middle age through young-old age to old-old age (Nyberg
379
et al., 2003).With aging, many aspects of information processing become less efficient, and both episodic
380
encoding and retrieval processes are impaired (e.g. Anderson et al., 2005; Giffard et al., 2001;Gutchess et al.,
381
2007; Morcom, 2003). Older individuals suffer from difficulties in retrievingthe encoding context and stored
382
information in a rich and detailed way; exhibit increases in the number of false recognitions; show decreases in
383
inhibition capacities that may be explained by problems with the self-initiated development of encoding
384
strategies(e.g., Bastin and Van der Linden, 2005; Fernandes and Manios, 2012).
385
The quality of the sensory information presented to the cognitive system (Craik and Rose, 2012) and the
386
duration it remains available for processing (Walsh and Thompson, 1978) can affect the encoding of memory in
387
older adults. EM is traditionally assessed using verbal memory tasks. The age-relateddecline in itsencoding was
388
supported by Park et al. (1989), who asked young and older adults to categorize words while performing a
389
number-monitoring task during encoding, retrieval or both. The authors found that the performances of older
390
adults were more highly impaired when their attention was divided during episodic encoding,whereas their
391
performance on retrieval tasks was similar to that of the young participants.Moreover, an insufficiently precise
392
and distinctive encoding can lead to false recognitions (e.g. Dennis et al., 2007b; Murphy et al., 2007; Rosa and
393
Gutchess, 2013), which arise mainly when new items presented during retrieval are closely related to those
394
encountered during encoding (e.g. Kensinger and Schacter, 1999; Koutstaal and Schacter, 1997).Recognition
395
tests that include semantic distractors (e.g. “dahlia” or “petunia” for the flowers category) yield more false
396
recognitions in the elderly than among young subjects. This suggests that general-level encoding allows the
397
elderly to reject semantically unrelated distractors (e.g. “camel”), whereas the correct discrimination of
398
semantically related items requires more elaborate encoding. In their meta-analysis, Spencer and Raz (1995)
399
reported that age had a differential effect on recall performances depending on the type of encoding (incidental
400
or intentional). Taconnat and Isingrini (2004) manipulated the conditions of encoding using the production
401
paradigm, which holds that memory is substantially benefited byproducing/generating the second word of a
402
word pair as opposed to just reading it. Young subjects were found tobenefit from both semantic and
403
phonological cues, while older subjects benefited from the production of the item only when there was a
404
semantic relationship between the item and the clue. This suggests that memory in the elderlycan benefit from
405
deep or semantic processing at encoding, but only when the conditions of encoding strongly guide the desired
406
operations. Finally, age-related deficits during encoding may also depend on the utilized stimuli. For example,
407
scene encoding tends to differ little with age because, unlike the recognition of words, that of non-verbal
408
material(e.g. pictures) is largely age-invariant (e.g.,Craik and Jennings, 1992; Gutchess et al., 2005; Park et al.,
409
1986).Individuals tend to better remember rich and meaningful stimuli (such as pictures) because such stimuli
410
automatically engage multiple representations and associations with other information about the world, leading
411
to more elaborate encodings (e.g., Craik and Rose, 2012).One possible explanation for the effects of normal
412
aging on EM results is the acquisition of a deficit in the strategic processes involved in encoding (Shing et al.,
413
2010). Indeed, the lower performance of the elderly on memory tests has been attributed to a lack of self-
414
initiated processes (Craik, 1990; Kausler, 1994; Sauzéon et al., 2000), whichleads to difficulties in implementing
415
the spontaneous cognitive operations required for optimal memory (Craik, 1986). Indeed, when verbal encoding
416
is incident or superficial,or where no task is requested, the elderly spontaneously engage in less effective
417
strategies. The task does not directly guide the subjects in establishing an encoding strategy; they must initiate it
12
418
by themselves, and their chosen strategy typically does not increase their memory performance (Guillaume,
419
2009; Taconnat and Isingrini, 2004; Van der Veen et al., 2006). For instance, Dunlosky and Hertzog (2001)
420
found that when subjects were given the freedom to choose a strategy from among four possibilities in order to
421
encode pairs of words, young subjects used more mental imagery and sub-vocal rehearsal strategies, whereas
422
older subjects tended to generate sentences with the two words or use no strategy at all. The authors proposed
423
thatthe performance decreases of middle ageseem to reflect a failure to initiate elaborate procedures rather than a
424
deficit in the encoding processes per se. After 60 years of age, encoding becomes less effective even in the
425
presence of aids and clues, and the mechanisms for developing and allocating attention are insufficient.When
426
environmental support is high, however, such individuals can process the information deeply. For example,
427
when old adults make a mental image, use a word in a sentence, or give a synonym during the encoding of a
428
word (Craik and Jennings, 1992), the memory trace is strong and durable; thisyields better test performance and
429
less performance difference between young and elderly participants (e.g.,Dunlosky et al., 2005; Froger et al.,
430
2009; Kalpouzos et al., 2009; Logan et al., 2002; Taconnat et al., 2008) regardless of the time spent studying the
431
items. In other words, a deep and semantic encoding, even performed over a relatively shortperiod, is more
432
effective than a superficial treatment made over a longer period (Craik and Tulving, 1975). The two factors of
433
“self-initiated processing” and “environmental support” are complementary, with less environmental support
434
meaning that more self-initiated processing must be deployed and vice versa.
435
Age-related memory deficits are also present during retrieval, and elderly people routinely forget things.
436
The interference theory (Dewar et al., 2007) suggests that such forgetfulnessreflects the similarities between
437
memorized materials, in that memory can be disrupted by what we have previously learned (old memories
438
interfere with the retention of new learning) or by what we will learn in the future (new learning interferes with
439
the retention of old memories). For example, it can be difficult to remember how to use an old phone when
440
learning to use a new one; this is an example of a competitive response leading to lower memory performance
441
(Blank, 2005; see also Fandakova et al., 2013).In the elderly, the degreeof the memory deficit varies depending
442
on the task:age-related differences are more pronounced in free recall tasks that require the subject to
443
spontaneously retrieve a previous episode without any external help, compared to cued recall or recognition
444
tasks, in which an index is provided to facilitate the mental research of the stimulus. The performances of older
445
subjects are inferior to those of young subjects during free recall, whereas the age groups are often equivalent
446
intheir recognition abilities(Craik and McDowd, 1987; Isingrini et al., 1996; Sauzéon et al., 2014; Taconnat et
447
al., 2009). These patterns of performance could be explained by insufficient encoding, in that the memory trace
448
is too weak to be reactivated during free recall but is sufficient for recognition. Old people have more difficulties
449
in spontaneously generating cues to retrieve information in memory (Dunlosky et al., 2005; Sauzéon et al.,
450
2001;), but they exhibit normal benefits from receiving semantic cues during such retrieval (e.g., Monti et al.,
451
1996).Work using the R/Kparadigm (Guillaume, 2009; Rajaram, 1993; Richardson-Klavehn et al., 1996) has
452
indicated that the elderly can have difficulty accessing the contextof learning (Bugaiska et al., 2007; Clarys et
453
al., 2002; Jacoby, 1991; Jennings and Jacoby, 1997; Prull et al., 2006). The ability to control the source of
454
information decreases with age, making subjects particularly vulnerable to false memories (Dodson and
455
Schacter, 2002; Johnson et al., 1993; Lövden, 2003). For example, Jacoby and Rhodes (2006) found that the
456
elderly were more likely to accept false information as true, compared to young adults. In addition, older
457
individuals had a greater sense of confidence in their misjudgmentscompared to young subjects (Dodson et al.,
458
2007). The proportion of Remember responses (R), which reflect the recovery of every contextual detail,
459
declines with aging, whereas the proportion of Know responses (K), which are associated with a sense of
13
460
familiarity, remains stable or increases slightly (e.g. Clarys et al., 2009).Older adults would therefore tend to
461
develop recovery processes based primarily on familiarity,but might struggle to identify the source of this
462
familiarity using contextual elements. In other words, age affects the quality and richness of the information
463
retrieved from memory. Fewer details are recalled and episodes are relived less frequently. This notion has been
464
reinforced by the observation of lower performance in the elderly on memory source tasks, compared to younger
465
subjects (Mitchell et al., 2003; Spencer and Raz, 1994).
466
In addition to strategic deficits, attention and processing speed may be critical components of the age-
467
related decline in EM function (see Park and McDonough, 2013). Craik (1986) hypothesized that the amount of
468
attentional resources available to initiate and carry out cognitive processes could decrease with age (Craik and
469
Jenning, 1992). The attentional demands of both encoding and retrieval are greater for older adults than for
470
young adults, although this age difference is most pronounced for retrieval (Craik and McDowd, 1987; Whiting
471
and Smith, 1997). Older subjects are less able to spontaneously develop the most effective encoding and retrieval
472
operations, because such operations are very expensive in terms of attention (Anderson et al., 1998). However,
473
other studies showed that the presence of a sufficiently large environmental context at the time of encoding (e.g.,
474
a semantic task) and/or retrieval (e.g., a clue) could minimize the need for a costly self-initiated treatment in
475
attention and reduce the memory impairment associated with age (Craik, 1986; Craik and Byrd, 1982).
476
The theory of cognitive slowdown proposes that changes in the processing speed significantly
477
contribute to age-related cognitive performance declines, leading to less effective encoding and increasing the
478
time required to retrieve stored information (Bunce and Macready, 2005; Clarys et al., 2002; Hertzog et al.,2003;
479
Perrotin et al., 2006; Salthouse, 1996).Indeed, when comparing elderly and young groups in recognition-based
480
retrieval, Daselaar et al. (2003) showed increased reaction times in the latter group, indicating that there is likely
481
to be an age-related slowing of motor responses. This model is based on the consistent observation that
482
processing speed shows a linear decrease during early adulthood, and that this decrease may accelerate in late
483
old age (Feyereisen & Van der Linden, 1997; Salthouse, 1993a, 1993b). Two distinct mechanisms appear to be
484
responsible for the relationship between processing speed and cognition:1) cognitive operations are performed
485
too slowly to be achieved in a limited time, and less cognitive processing is generally associated with a lower
486
level of performance; and 2) the slowdown reduces the amount of available information, which isneeded for the
487
execution of higher-level cognition.In the elderly, this slowdown primarily affects the encoding operations,
488
resulting in the creation of fragile memory representations.
489
It has also been established that normal aging is accompanied by a decrease in an individual’s capacity
490
to inhibit the acquisition of irrelevant information on the verbal, motor, attentionalandmnesic levels (Connely et
491
al., 1991; Potter and Grealy, 2006; Spieler et al., 1996).The inhibitory capacity can be defined as the set of
492
sequential processesimplemented to prevent the emergence of an automatic or context-induced response, or
493
(conversely) to prevent irrelevant information from entering theattentional field. However, the performance of
494
the elderly can reportedly becomparable to that observed in young subjects,indicating that not all aspects of
495
inhibitory function undergo age-related alterations. For example,Jennings and Jacoby (1993) demonstrated that
496
some age-related memory differences are due to declines in controlled (but not automatic) information
497
processing for verbal (Healy et al., 2005) or non-verbal (Zelazo et al., 2004)materials (see also Hasher and
498
Zacks, 1979;Jacoby et al., 2001; Yonelinas, 2002). Indeed, the concept of controlled retrieval implies that there
499
is an intentional effort to initiate research in memory and consciously control and mobilize attention throughout
500
the task, all of which are costly processes.
14
501
In
sum,
normal
aging
is
usually
accompanied
by
declines
in
various
behavioral
502
performanceseitherduring encoding or retrieval or even during both phases according to the stimuli, the
503
paradigm, the environment and the strategies used by the person.Nevertheless, a change in the organization of
504
the neural networks underlying EM can also be responsible for the difference seen between young and older
505
adults.
506
4/ Chemical and anatomical data: role of brain imaging study in healthy elderly
507
The age-related decline in EM seems to reflect the depletion of neurotransmitters as well as age-related
508
degradation of the brain’s anatomy and physiology (Coleman and Flood, 1987; for review, see Grady, 2012).
509
Recently, the advent of non-invasive neuroimaging methods (e.g., fMRI and PET) has enabled researchers to
510
examine normal memory processes in the healthy brain (Spaniol, 2009), yielding a better understanding of the
511
links between cognitive skills and neural substrates. The earliest cognitive and neuroanatomical information
512
about EM originated from the study of patients suffering from amnesic syndrome or frontal lesions (Squire,
513
1992). Indeed, if these patients do not have real amnesic syndromes, they experience similar difficulties than
514
older subjects. Older adults, as brain-frontal subjects, exhibit more intense deficits in memory tasks that require a
515
significant contribution by controlled processes, such as free recall.
516
Investigations using non-human primates and neuropsychological approaches have revealed activation
517
patterns that indicate the existence of a relatively wide neuronal network underlying EM (Andreasen et al., 1995;
518
Cabeza et al.,1997; Cabeza and Nyberg, 2000; Desgranges et al., 1998; Nyberg et al., 1996a; Nyberg et al.,
519
1996b; Rugg and Vilberg, 2013; Shimamura, 2014). It mostly comprises the PFC, the MTL and particularly the
520
hippocampus but also the parietal cortex.Neurofunctional changes in these regions also seem to be correlated
521
with age-related memory declines and learning difficulties (Head et al., 2009; Raz, 2000; Raz et al., 2005;
522
Yonelinas et al., 2007). For example, Rajah and colleagues (2011) found that age-related reductions in the
523
volume of the medial frontal gyrus were negatively correlated with retrieval activity in the same regions during
524
an EM task.
525
4.1/ Depletion of neurotransmitters
526
With respect to disorders of neurotransmission associated with cerebral aging, converging arguments
527
indicate that dopamine deficiency is the main neurobiological determinant of the aging brain. DA function has
528
traditionally been linked to motor performance (Freed and Yamamoto, 1985) and reward-related processes
529
(Baudonnat et al., 2013; Schultz, 2006; Wise, 2004). Authors demonstrated that DA is truly a learning signal
530
(Schultz, 1998) and is invoved in learning of a stimulus-reward association (Waelti et al., 2001). This
531
neurotransmitter codes for incentive salience, the neural process that generates the desire and motivates an
532
individual to act in order to get the reward (Berridge and Robinson, 1998). For example, mice deprived of DA
533
are still sensitive to rewards but fail to motivate their behavior. In monkeys, DA amplitude discharges better
534
correlate with the level of motivation than with the size of the reward (Satoh et al., 2003).More recently, DA has
535
been associated with higher cognitive abilities, such as attention and memory processes (Starter and Bruno,
536
2004), in patient populations with severe damage to the DA system, such as those afflicted with Parkinson
537
Disease and Huntington Disease (Brown and Marsden, 1988), as well as in lesion studies in monkeys (Goldman-
538
Rakic, 1998), and pharmacological studies using DA agonists in younger volunteers (Luciana et al., 1998).
15
539
Functional neuroimaging studies have demonstrated that interaction between reward-related regions
540
(orbitofrontal, ventral tegmental areas, striatum, PFC or substantia nigra) and memory-related regions including
541
the MTL structures, could contribute to the memory enhancement by reward motivation (e.g., Tsukiura and
542
Cabeza, 2008; Wittmann et al., 2011; Wolosin et al., 2012). Some studies have shown that reward improves
543
memory formation in incidental and intentional encoding paradigms (Wittmann et al. 2005; Adcock et al. 2006;
544
Callan and Schweighofer 2008; Wittmann et al. 2008). Others demonstrated that higher-value (i.e. high
545
monetary reward) items are remembered better than low-value items (i.e. low monetary reward) (e.g. Adcock et
546
al., 2006; Wittmann et al., 2005; Shigemune et al., 2010). Nevertheless, Madan and Specth (2012) recently
547
reported that memory is enhanced not only due to reward value but also to reward salience (highest and lowest
548
value items are remembered best and intermediate-value items are remembered worst). Reward has also been
549
demonstrated to abolish the so-called « Retieval-Induced Forgetting » (Imai et al., 2014), a memory phneomenon
550
where remembering causes forgetting of other information in memory. It is believed to prevents us from
551
becoming confused between information we’ve made an effort to learn and closely related information we didn’t
552
strive to learn. Reward overall enhanced memorized items and abolished the suppression of the retrieval of non-
553
learned items. However, a depletion of DA can have a consequence on the « reward –effect ». Lesion of some
554
dopaminergic pathways (e.g. nigrostriatal pathway), as well as pharmacological blockade of DA receptors,
555
makes the animals insensitive to rewarding effects, result in a lack of interest for environmental stimuli and a
556
decrease in exploratory behavior (Di Chiara, 2002; Wise, 2008). The duration of reward was reduced by
557
dopaminergic antagonists (Yokel and Wise, 1975; 1976). DA depletion has also been linked with reward theory
558
in healthy aging. Indeed, Dreher and colleagues (2008) demonstrated that the coupling of midbain DA synthesis
559
and reward-related PFC activity was altered in older adults. DA reward reponse appears to code the discrepency
560
between the reward and its prediction. This « prediction-error » seems to be altered in older adult, resulting in an
561
abnormal signature of expected value and then an incomplete reward prediction error signal. Chowdhurry and
562
her colleagues (2013) found that this abnormal reward procesing in aging can be restores with DA (see also
563
Eppinger et al., 2011). Healthy aging has also been show to induce functional altertions in the reward system
564
Wong et al. (1997) found a decrease in the number of dopaminergic receptors with age. In vivo studies
565
using PET found smaller (but reliable) age-related declines in the human striatum, responsible for a large
566
proportion of DA production. This area has extensive connections to the PFC (Graybiel, 2000)and might
567
therefore affect the cognitive processes that are sub-served by DA-dependent circuits (Hedden and Gabrieli,
568
2004). Post-mortem evidence indicates that age induces substantial losses in both pre- and postsynaptic markers
569
of the DA system (Fearnly and Lees, 1991). Likewise, PET findings demonstrate marked age-related decreases
570
in DA function for presynaptic markers, such as L-DOPA utilization and DA transporter density (VanDyck et
571
al., 1995; Volkow et al. 1996) as well as for postsynaptic markers, such as D1 and D2 receptor binding. Age-
572
related decreases in performance were significantly correlated with D2 receptor availability and binding
573
(Bäckman et al., 2000; Erixon-Lindroth et al., 2005). Furthermore, intermittent stimulation of dopamine D1
574
receptor systems was shown to improve delayed response performance for older monkeys while having a small
575
detrimental effect for young monkeys. These beneficial effects remained in effect at 1 year following
576
stimulation. Dopamine stimulation might thus specifically benefit populations with deficiencies (older adults)
577
and could provide the basis for treating even normal age-related declines (Castner and Goldman-Rakic, 2004). In
578
a pharmacological fMRI study, Morcom et al. (2010) showed that elderly subjects with worse recognition
579
performance scores on EM tasks were more sensitive to dopaminergic modulation induced by bromocriptine (a
580
D2-like receptor agonist) or sulpiride (a D2-like receptor antagonist), as reflected by activity in the left MTL
16
581
during efficient EM encoding. Age-related losses of DA have also been observed in non-striatal structures,
582
including the frontal, temporal and occipital cortices, as well as the hippocampus and thalamus (Inoue et al.,
583
2001; Kaasinen et al., 2000).
584
Acetylcholine is another neurotransmitter that plays an important role in memory (Deutsch, 1971; Gold,
585
2003; Hasselmo, 1999; 2006). The two main subtypes of cholinergic receptors, nicotinic and muscarinic, are
586
both sensitive to the effects of age (Giacobini, 1990; Nordberg et al., 1992), and cholinergic deficiency has been
587
suggested to explain at least part of the age-related declines in memory performance (Gallagher and Colombo,
588
1995; Taylor and Griffith, 1993). Memory performance decreases comparable to those observed in elderly
589
subjects were demonstrated in young subjects after scopolamine-induced blockade of muscarinic receptors
590
(Jones et al., 1991), but it is not yet known whether a cholinergic deficit can affect memory directly, or indirectly
591
alter it by disturbing attention (Blokland, 1995; Everitt and Robbins, 1997; Hasselmo and Bower, 1993; Voytko,
592
1996). In a resting-state fMRI study, Wink et al. (2006) found that the administration of scopolamine to young
593
healthy subjects mimicked the dynamics of hippocampal activity observed in placebo-treated elderly subjects,
594
suggesting that a cholinergic mechanism may underlie the age-related changes in EM.
595
4.2/ Prefrontal cortex
596
The results from brain imaging and behavioral studies on age-related morphological brain changes
597
converge to suggest the presence of critical alterations in the PFC brain region, which is associated with
598
executive functions (West, 1996; Kalpouzos et al., 2009). This supports the frontal hypothesis, which holds that
599
executive functions are the first cognitive functions to decline during aging, leading to the strongest and earliest
600
age-related changes in the cognitive skills that depend on such functions (Taconnat et al., 2007). With respect to
601
memory, declines in executive function impair strategic, controlled processing at the levels of encoding and
602
retrieval. Memory profiling of frontal brain-damaged patients and neuroimaging studies have shown that there is
603
a close link between memory (especially EM) and frontal activity (Cabeza, 2002). The frontal lobes play key
604
roles in acquiring and encoding information, retrieving information in the absence of contextual cues, recalling
605
the source of information, and assessing the temporal sequence and recency of events. Relevant functional
606
dissociations have been found within the frontal cortex (e.g.,Blumenfeld and Ranganath, 2006, 2007; Rypma and
607
D’Esposito, 2003); the ventrolateral region contributes to selecting appropriate information, while the
608
dorsolateral area organizes the information in working memory. These two regions thus play complementary
609
roles leading to the formation of EM.
610
4.3/ From HERA to HAROLD: the compensation models
611
Kapur et al. (1994) used PET to study EM in 12 healthy volunteers and observed important activations
612
of the left inferior PFC (Brodmann areas 45, 46, 47 and 10) during an encoding task and the right dorsolateral
613
frontal cortex (Brodmann areas 10, 46, 9) during a recall task. This asymmetry led scientists to propose the
614
HERA (Hemispheric Encoding/Retrieval Asymmetry) model (Tulving, 1994), which holds that the left frontal
615
cortex is preferentially involved in episodic encoding, whereas the right frontal cortex is preferentially involved
616
in episodic retrieval. Others studies also found unilateral activity in young adults (e.g., Cabeza et al., 2004; Davis
617
et al., 2012; de Chastelaine et al., 2011; Reuter-Lorenz et al., 2000; Schneider-Garces et al., 2010; for reviews,
618
see Cabeza and Nyberg, 2000; Fletcher and Henson, 2001). Regions in the left PFC are consistently activated
17
619
during the encoding of non-verbal material (e.g., object localization, Ownen et al., 1996; unknown faces, Grady
620
et al., 1995). Conversely, right PFC activation is seen during the retrieval of episodic information (Morcom et
621
al., 2003), as extensively demonstrated with paradigms using free recall, cued recall, or recognition of diverse
622
stimuli, such as sentences, drawings of objects, words, faces, smells, melodies, and colored geometric patterns
623
(e.g., Nyberg et al., 1996; Bernard et al., 2001; Platel et al., 2003). Notably, however, some authors have failed
624
to confirm these results and found bilateral recruitment of the PFC (e.g., Kelley et al., 1998; Spaniol, 2009). It
625
was suggestedthat the PFC is bilaterally recruited when a task requires increased cognitive resources (Cairo et
626
al., 2004; Nolde et al., 1998), thereby showing a pattern similar to that observed in older adults during the
627
performance of simpler tasks. In 1998, Nyberg proposed that parts of the right PFC should be distinguished into
628
the right anterior PFC, which is involved in all memory tasks, and the right posterior PFC, which is involved in
629
the more difficult retrieval operations. Together, these findings suggest that the HERA model is modulated by
630
the nature of the material (Fliessbach et al., 2006; Golby et al., 2001; McDermott et al., 1999; Wagner et al.,
631
1998), the complexity of the task (Nolde et al., 1998) and the involved memory process (e.g., Iidaka et al., 2000;
632
Nyberg et al., 2000).
633
Given the imaging studies showing the consistent involvement of PFC regions in memory among
634
younger adults and their central role in cognitive aging, it is of critical interest to study PFC activity in the
635
elderly. The structural and behavioral data discussed above suggest that one might expect neural activity to
636
decline with age (e.g., Logan et al., 2002; for review, see Park and Gutchess, 2004), consistent with the declines
637
in cognitive function and brain structure. Quite surprisingly, numerous neuroimaging studies of EM have shown
638
that the functional brain activity in the PFC increases with age across a range of tasks, with increases in right
639
frontal areas and reductions in left frontal activity during encoding(e.g., Anderson et al., 2000; Cabeza, 1997;
640
Grady et al., 1995; 2002; Leshikar et al., 2010; Morcom, 2003; Nyberg, 1996a, 1996b; Rosen et al., 2002; for
641
review, see Dennis & Cabeza, 2008) and vice versa during EM retrieval. This bilateral pattern of PFC activity in
642
the elderly reduces their hemispheric asymmetry, as reflected in the HAROLD model (Hemispheric Asymmetry
643
Reduction in OLDer Adults) proposed by Cabeza (2002). Additional prefrontal recruitment is tought to be a
644
general characteristic of age-related neural change (Cabeza et al., 2004; Davis et al., 2008; for review, see
645
Spreng et al., 2010). This lack of asymmetry is observed in a wide range of tasks, including word recall after
646
incidental learning (Logan et al., 2002; Stebbins et al., 2002), intentional learning (Logan et al., 2002), delayed
647
recall (Morcom et al. 2003), and memory retrieval (Bäckman et al., 1997; Hatta et al., 2015). But in the field of
648
pictorial stimuli in young subjects, older adults cannot engage bilateral regions as predicted by the HAROLD
649
model as both hemispheres are already activated in young adults (Golby et al., 2001; Kelley et al., 1998).
650
Gutchess et al. (2005) hypothesized that older adults would show increased prefrontal activations in regions not
651
activated by young adults. While both young and older adults showed bilateral activations of the inferior frontal
652
gyri during the successful encoding of pictures of outdoor scenes, the older adults showed more activation of
653
several other frontal regions (including the left middle frontal gyrus) compared to younger subjects.
654
Two interpretations have been proposed to account for the HAROLD phenomenon in aging. In the
655
absence of memory decline in elderly people, a more widespread activation pattern is interpreted as reflecting
656
either: 1) difficulty in engaging specialized neural mechanisms, which is a phenomenon called
657
“dedifferentiation” (e.g., Li and Lindenberger, 1999; Logan et al., 2002); and/or 2) an optimized cognitive
658
mechanism (i.e., the use of a cognitive strategy different from that of younger adults) to deal with the executivo-
659
frontal dysfunction that accompanies normal aging (Reuter-Lorenz and Lustig, 2005; Stern et al., 2009; for
660
review, see Cabeza, 2004). The latter compensation phenomenon suggests that older individuals engage both
18
661
hemispheres in some tasks that require only one hemisphere in young subjects; this compensates for cognitive
662
deficits, and is thus positively correlated with successful cognitive performance (Reuter-Lorenz et al., 2000; Park
663
et al., 2003). Concerning encoding, the age-related shift from left lateralized processing to a more distributed
664
pattern corresponds not only to encoding attempt, but mostly ultimate success. Indeed, activating a second
665
hemisphere would increase the resources that the elderly have available (Ska, 2006) to generate the same
666
functional result as their younger peers (Cabeza et al., 2002, 2004). This additional frontal recruitment allows
667
older adults to maintain a good level of accuracy at the expense of a slower reaction time (Grady et al., 1994; but
668
also see Reuter-Lorenz et al., 2000). Some studies have suggested that age-related over-recruitment is observed
669
in only a few PFC regions, such as the bilateral medial and superior frontal gyri (Gutchess et al., 2005), and in
670
the bilateral anterior superior frontal gyri (Morcom et al., 2003). In contrast, bilateral activation of the PFC in
671
older adults is not always related to better performance. In a recent review (2012), Grady reported that some
672
authors found greater recruitment in the PFC during memory encoding (de Chastelaine et al., 2011) and retrieval
673
(Persson et al., 2011) in elderly participants, but this was correlated with poorer memory. Similar results were
674
obtained during word recognition (Madden et al., 1999), facial recognition (Grady et al., 2002), and spatial tasks
675
(Piefke et al. 2012; Meulenbroek et al., 2010).
676
In a PET study, Bernard et al. (2007) tested young and elderly subjects in a cued recall task. The
677
activation of the right PFC was similar in the two groups, but there was a significant between-group difference at
678
a behavioral level, with the older subjects showing lower-level performance. This apparent paradox was solved
679
by taking into account the results of a previous study in which two groups of older subjects were scanned while
680
performing episodic retrieval of verbal material: a group of “low-performers” with significantly lower episodic
681
retrieval performances compared to young healthy subjects; and a group of “high-performers” with
682
performances comparable to those of young subjects (Cabeza et al., 2002). Similar to the young participants, the
683
low performers showed activation of only the right PFC. In contrast, the elderly high-performers showed
684
activation of both the right and left PFC, suggesting that their brains were working harder and engaging in a
685
more distributed compensatory process. According to Park (2009), the additional activation of the contralateral
686
hemisphere reflects the inefficient operation of inhibitory mechanisms. Overall, these results suggest that there is
687
a three-way interaction among age, task difficulty, and fontal laterality.
688
A variety of theoretical models have been proposed to explain age-related over-recruitment (e.g.,
689
Cabeza and Dennis, 2013; Davis et al., 2008; Maillet and Rajah, 2013). The age-related decreases in brain
690
structure size and white matter integrity concomitant with increases in prefrontal activation prompted the
691
development of the Scaffolding Theory of Aging and Cognition (STAC; Park and Reuter-Lorenz, 2009), which
692
describes the brain’s response to cognitive challenge. This model posits that despite neural challenges and age-
693
related worsening, behavior is maintained at a relatively high level by the recruitment of additional circuitry.
694
With age, this compensatory scaffolding process may be invoked to perform familiar tasks and basic cognitive
695
operations, which become increasingly challenging as the existing neural circuitry degrades. In addition, the
696
over-recruitment of the PFC may reflect an attempt to compensate for age-related declines in other brain regions
697
(Cabeza et al., 2004; Gutchess et al., 2005; Goh et al., 2010). For example, the PASA model (Posterior-Anterior
698
Shift in Aging) (for review, see Davis et al., 2008) suggests that a decrease in posterior cortical activations (i.e.,
699
that of the occipito-temporal cortex) in older adults is accompanied by an increase in anterior activity,
700
particularly frontal. Some recent work suggests that PASA patterns may be particularly prevalent under more
701
taxing cognitive demands (Ansado et al., 2012), but the recruitment of additional brain regions might come with
702
a cost (Bäckman & Dixon, 1992; Cabeza, 2002; Reuter-Lorenz et al., 2008). For example, the recruitment of
19
703
contralateral hemispheres may reduce the brain’s ability to perform simultaneous tasks. Given that older brains
704
engage more neural circuitry at lower levels of task demand compared to younger brains, seniors rely more
705
heavily on their CR and are more likely to reach a limit on the resources that can be brought to bear on task
706
performance. Reuter-Lorenz and Cappell (2008) referred to this as CRUNCH (Compensation-Related Utilization
707
of Neural Circuits Hypothesis).
708
In applying the PFC function theory to cognitive aging, the work of West (1996) supported the
709
hypothesis that cognitive processes supported by the PFC are among the first to decline with increasing age.
710
However, differences were also observed on tasks that are traditionally considered to be “non-frontal” (e.g., item
711
recall and recognition), leading West to conclude that: “this age related decline in item recall and recognition
712
suggests that the frontal lobe hypothesis of aging provides a useful but incomplete neuropsychological model of
713
cognitive aging.” Some investigators have pointed out that the performance of memory tasks involves the
714
coordination of multiple neural systems beyond the prefrontal cortex. Indeed, the frontal hypothesis (which is
715
admittedly somewhat simplistic) should not obscure the roles of other brain structures (e.g., the parietal cortex),
716
especially when the real memory difficulties among older subjects could be better explained by MTL
717
dysfunction.
718
4.4/ Aging in the PFC: link with behavioral data
719
The HAROLDfinding was more prevalent in intentional versus incidental encoding studies, suggesting
720
that the environmental support provided by a deep encoding task may attenuate the age-related decreases in left
721
PFC activity (Daselaar et al., 2003; Dennis and Cabeza, 2008; Kapur et al., 1996; Logan et al., 2002; Morcom et
722
al., 2003). Nevertheless, a PET study by Bernard et al. (2001) showed that the intentional encoding of words
723
bilaterally activated the PFC, with a larger activation noted in the left hemisphere. Similarly, deep processing of
724
pictures triggered increased activity in the left PFC and bilateral medial temporal regions (Grady et al., 1999).
725
Deeper processing (e.g., semantic judgment tasks) was also shown to activate the inferior PFC and left
726
dorsolateral PFC (DLPFC) more strongly than a more shallow treatment (Demb et al., 1995; Fujii et al., 2002;
727
Iidaka et al., 2000; Otten et al., 2001; for review, see Galli, 2014). In an associative encoding task, older adults
728
showed a typical pattern of increased activity in the right inferior frontal region, the left inferior frontal gyrus,
729
and the left hippocampus as the task difficulty increased (Leshikar et al., 2010). Furthermore, activity in these
730
regions has been found to predict subsequent memory performance (Wagner et al., 1998; for review, see Park et
731
al., 2013). In young adults, activity in the PFC was found to predict the formation of successful memory (Brewer
732
et al., 1998; Kirchhoff et al., 2000), while a subsequent memory task showed that increased frontal activation in
733
older adults was associated with remembered items, but not with forgotten items (Gutchess et al., 2005).
734
Mitchell et al. (2004) also observed that young adults showed activation in the left
735
judgments, whereas older adults did not. The authors posited that the source memory deficits seen in older adults
736
might be related (at least in part) to reductions in the function of the left PFC region that is engaged by young
737
adults. Thus, the left PFC appears to be specifically involved in more complex memory tasks or those that
738
require encoding strategies (Fletcher and Henson, 2001). Patients with left frontal lesions present specific
739
deficits when the task requires semantic strategies during encoding (e.g., Incisa della Rocchetta and Milner,
740
1993), whereas their performances returned to normal when they were provided with semantic clues or
741
instructions on the use of specific strategies (Gershberg and Shimamura, 1995). Thus, one important function of
742
the PFC in memory is to focus behavior towards the development of a strategy aimed at optimizing memory
DL
PFC during source
20
743
performance. Specifically, the encoding-related activity in the ventrolateral PFC (VLPFC) is believed to reflect
744
the selection, maintenance, and control of incoming information (Blumenfeld et al., 2011), whereas activity in
745
the
746
Ranganath, 2007; Daselaar et al., 2006; Paller and Wagner, 2002; Simons and Spiers, 2003). Other studies have
747
emphasized the content-specific aspects of prefrontal function, with left-lateralized ventrolateral activity
748
appearing to be associated with verbal material and right-lateralized activity with visual material (Wagner et al.,
749
1998).
DL
PFC is thought to support organization and associative encoding (for reviews, see Blumenfeld and
750
Lepage et al. (2000) identified a set of regions associated with the “retrieval mode” (REMO) in EM.
751
The activation of the REMO sites is described as governing the subject’s neurocognitive state when the attention
752
is focused on a segment of the past; this state takes into account the relevant indices, inhibits the irrelevant
753
indices and supports effective access to the memory trace. The REMO sites include the anterior cingulate cortex
754
and various frontal regions, and are preferentially lateralized to the right. Several studies found regions that were
755
similarly activated by recognition across age groups (Daselaar et al., 2003; Tisserand et al., 2005), leading
756
researchers to suggest that age effects are more pronounced for encoding than retrieval. However, age-
757
differences are still seen in the latter. Several studies found decreased activity in the right PFC in older adults
758
(e.g., Anderson et al., 2000; Cabeza et al., 1997; Bäckman et al., 1997); this frontal under-activation was greater
759
for source recall tasks than for recognition tasks, suggesting that reductions in right frontal activity might be
760
proportional to the difficulty of the task. Whereas the left
761
anterior PFC regions are more strongly involved in retrieval (Spaniol, 2009). Sub-regions of the PFC have been
762
implicated in various retrieval-related functions, including setting the retrieval mode, specifying retrieval cues,
763
and post-retrieval monitoring and verification (e.g., Burgess et al., 2007; Cabeza et al., 2003; Dobbins and Han,
764
2006; Moscovitch and Winocur, 2002; Rugg et al., 1998; Shallice, 2002; Simons and Spiers, 2003). The first two
765
aspects are more dependent on the
766
DL
767
in older subjects compared to young subjects. In addition, various frontal sub-regions have been demonstrated to
768
be differentially involved in recollection (R) and familiarity (F) (for review, see Skinner and Fernandes, 2007).
769
Both have been associated with right
770
the anterior frontal (related to source information) and superior frontal (related to attentional processes) regions.
771
In the future, it should be interesting to determine how the frontal lobe sub-regions contribute to different
772
processes related to R- and F-based responses.
773
VLPFC,
VLPFC
was more strongly involved in encoding,
whereas monitoring and verification are more dependent on the
PFC. Schacter et al. (1996) found that frontal activity during recall of word pairs was located more posteriorly
DLPFC
activity, while R is associated with additional bilateral activity in
4.5/ Medial temporal lobes
774
Following Scoville and Milner’s (1957) report on amnesic patient HM, human and animal lesion work
775
focused intensively on the role of the hippocampus and surrounding MTL in memory (for review, see Annese et
776
al., 2014; Rosenbaum et al., 2014). Vargha-Khadem et al. (1997; 2001) noted that severe EM disorders were
777
associated with congenital bi-hippocampal lesions. This structure operates by forming associations among the
778
sensory, cognitive and emotional processes that make up an episode in memory (Eichenbaum, 1996; see also
779
Hannula et al., 2006; Holdstock et al., 2005). The MTL has been the subject of much research in this area, both
780
because it plays a key role in EM function (for reviews, see Cabeza and Nyberg, 2000; Desgranges et al., 1998)
781
and because it is usually the first structure targeted by AD lesions (for review, see Dickerson and Eichenbaum,
782
2010). This structure seems to be involved in novelty detection (e.g., Dolan and Fletcher, 1997), and in encoding
21
783
and conscious retrieval of information (Wheeler et al., 2004). Notably, more severe age-related declines have
784
been associated with decreased activity in the MTL during encoding (Daselaar, 2003; Spaniol, 2009; Tisserand
785
et al., 2005).
786
The left-sided activation of the temporal and cingulate areas in encodingtasks reflects an asymmetrical
787
activation that fits the HERA model, but also seems to depend on the material in question (Desgranges et al.,
788
1998). For example, MTL is bilaterally activated during the encoding of digitized topographic information
789
(Aguirre et al., 1996), and the intentional encoding of complex images (Stern et al., 1996), while right
790
hippocampal activation was observed during face learning (Grady et al. 1995). Indeed, the results for this
791
structure are divergent. Some studies have found atrophy of the hippocampal region (Tisserand et al., 2004), and
792
less activity during memory encoding (Spreng et al. 2010) and retrieval in the elderly compared to young healthy
793
subjects (Dennis et al., 2007; Gutchess et al., 2005; Morcom et al., 2003; St Jacques et al., 2009). Decreased
794
medial-temporal involvement among elderly subjects has been reported in a number of tasks, including the
795
encoding of faces (Grady et al., 1995), verbal materials (Daselaar et al., 2003) and natural scenes (Park et al.,
796
2003). Age-related under-recruitment is believed to contribute to the age-related deficits observed in EM
797
performance. For example, when Daselaar et al. (2003) divided older adults according to their performance, low
798
performers showed less hippocampal activity than high performers. Moreover, reduced MTL function is often
799
accompanied by increased activation in the frontal cortex (i.e., PASA). Other studies have shown a relative
800
preservation (Good et al., 2001 Miller et al., 2008; Persson et al., 2011; Sullivan et al., 2005) and left MTL
801
activation during encoding was shown to predict successful memory retrieval performance in both young and
802
older subjects (Bernard et al., 2007). The apparent discrepancies in such results may reflect the encoding process
803
used. For example, Grady et al. (1999) observed bilateral recruitment of MTL regions when they focused on
804
subsequent memory, whereas Spreng et al. (2010) studied episodic encodingand noted reduced activity in the
805
right MTL of older adults. Alternatively (or in addition), the age range of the selected subjects may explain the
806
between-study differences: for samples covering a wide age range, the results tend to favor the preservation of
807
the structure, whereas studies focusing on narrower age ranges, especially patients over 50 or 60 years, found
808
atrophy of the hippocampus (for review, see Barbeau, 2011).
809
Based on the finding that elderly adults typically benefit less than young adults from deep processing of
810
study items, age-related impairments in EM are believed to be related to deficiencies in semantic processing
811
during encoding. For example, Daselaar et al. (2003) used fMRI on groups of young and elderly adults,
812
comparing brain activity patterns obtained during deep (living/non-living) and shallow (uppercase/lowercase)
813
encoding tasks. Although other regions were commonly activated during both processes, older adults revealed
814
significantly less activation in the left anterior hippocampus during deep processing but not shallow processing
815
compared to the young. This suggested that deep processing activates the MTL in young subjects but not older
816
subjects, further suggesting that there may be an age-related dysfunction of the posterior portion of the
817
hippocampus (Kalpouzos et al., 2008).
818
The findings from PET studies converge to the observations made by Lepage et al. (1998), who stated
819
that episodic encoding is almost exclusively associated with the anterior caudal region of the MTL, particularly
820
the hippocampus, whereas more posterior rostral (though not necessarily hippocampal) MTL regions play a
821
stronger role in episodic retrieval. Thus, the hippocampus may not function exclusively in the encoding or
822
recalling of events. For both encoding and retrieval, neural activations are located preferentially in the left
823
hemisphere for verbal material and in the right or both hemispheres with non-verbal stimuli (Davachi, 2006).
824
This rostro-caudal gradient, which is referred to as the HIPER (HIPpocampal Encoding/Retrieval) model,
22
825
(Lepage et al., 1998) seems to hold for verbal and non-verbal materials, and largely for both hemispheres too,
826
especially during retrieval, when the activations produced by the two stimulus types are distributed more or less
827
evenly in both hemispheres. The situation is less clear for the encoding of verbal information, as researchers
828
noted an absence of associated activation in the right hippocampal region. Furthermore, some studies have failed
829
to support the distinction of an anterior-posterior gradient. For example, Greicius et al. (2003) found that the
830
middle and posterior parts of the hippocampus are associated with both the encoding and retrieval of episodic
831
information. Moreover, other studies contradicted that of Lepage by showing that: 1) the anterior part of the
832
MTL is more strongly involved in retrieval, whereas the posterior part is associated with encoding processes
833
(Gabrieli et al., 1997; Rombouts et al., 2001; Schacter & Wagner, 1999); and 2) encoding activations in PET are
834
observed frequently in both anterior and posterior MTL sites, with a less clearly defined tendency for a
835
rostrocaudal gradient. In light of these results, it is then important to determine why episodic encoding involves
836
both the anterior and posterior MTL, whereas episodic retrieval is mainly associated with the posterior region
837
(Madden et al., 1999). In general, age-related changes in MTL activity are consistent with the associative deficit
838
theory, which posits that age-related memory deficits primarily reflect difficulties in encoding and retrieving
839
novel associations between items (Chalfonte and Johnson, 1996; Naveh-Benjamin, 2000;). Given that relational
840
memory has been strongly associated with the hippocampus, this hypothesis predicts that older adults will show
841
decreased hippocampal activity during memory tasks, particularly tasks that involve associations.
842
Some authors have favored the idea that the medial temporal cortex mainly functions in the recall of
843
episodic information (Ekstrom and Bookheimer, 2007), while other studies have contradicted this notion
844
(Cabeza et al., 1997). According to Schacter et al., (1996), the absence of hippocampal activation in some
845
studies seems to be related with the nature of the utilized tasks, with primary involvement of the PFC observed
846
when the task requires a highly demanding research strategy. The involvement of the hippocampus has been
847
demonstrated during the retrieval of episodic information with respect to verbal material (Rugg et al., 1997;
848
Schacter et al., 1996), drawings (Schacter et al, 1995), and topographical information (Owen et al., 1996). A
849
growing body of literature describes the neural structures underling recollection and familiarity in healthy
850
individuals. Within the MTL, studies have distinguished between the hippocampus and the parahippocampal
851
gyrus (Shastri, 2002): the former appears to be related to both recollection and familiarity (Aggleton and Brown,
852
1999; Mayes et al., 2002), and is reduced in older adults; the latter, in contrast, is related to familiarity and shows
853
increased activity in the elderly relative to younger subjects (Bäckman et al., 1997; Daselaar et al., 2006; Skinner
854
& Fernandes, 2007; Yonelinas, 2001; but also see Stark and Squire, 2003). This conclusion is supported by the
855
R/K paradigm, wherein subjects must specify under which circumstances the information was encoded (i.e., with
856
or without revival). Hippocampal activation is lower in the elderly compared to younger subjects, reflecting the
857
importance of the hippocampus in the more elaborate aspects of EM. In contrast, the rhinal and perirhinal
858
cortices (located near the hippocampus) show greater activity in older subjects, suggesting that this region
859
underpins another, less fragile aspect of memory: the feeling of familiarity (Daselaar et al., 2006; Vanssay-
860
Maigne et al., 2011). These results are in line with the fact that elderly people show greater impairments in
861
recollection than in familiarity (e.g., Cabeza et al., 2004; Jennings and Jacoby, 1993; but also see Rosenbaum et
862
al., 2014, patient NB), and suggest that the elderly rely more heavily on familiarity to compensate for the deficit.
863
These findings also indicate that older adults compensate for hippocampal deficits by relying more on the rhinal
864
cortex, possibly through a top-down frontal modulation. This is consistent with the fact that older people present
865
a larger portion of “Know” responses than younger adults. In sum, during episodic retrieval, both decreases and
866
increases in MTL activity may be seen, depending on the involved sub-region(s).
23
867
4.6/ Are other neural substrates of EM affected by age?
868
In addition to the PFC and MTL regions, neuroimaging studies have also implicated the parietal cortex,
869
the cingulate gyrus, the retrosplenial region, the amygdala and the cerebellum in EM (Desgranges et al., 1998;
870
Spaniol, 2009). The effects of aging on these brain structures have not yet been established, but the parietal
871
neocortex has been increasingly accepted as being involved in the age-related declines of EM (Desgranges et al.,
872
2008; for review, see Wagner et al., 2005). As proposed Nyberg et al. (1996) with respect to young subjects, the
873
asymmetry described by the HERA model may hold true for other brain regions, becoming a “HERA extended”
874
model. The encoding of episodic information activates the left parietal cortex during object localization, and
875
Sperling et al. (2003) found that parietal activation during the encoding of novel face–name pairs was higher in
876
elderly participants versus young controls. In contrast, however, bilateral or right-side activations of the parietal
877
cortex have been associated with retrieval (Desgranges, 1998). In a category-learning task, older adults showed
878
greater bilateral parietal activation compared to young adults, and this bilateral activity was associated with
879
higher performance (Fera et al., 2005). This age-related over-recruitment also appears to be compensatory,
880
perhaps improving the ability of older adults to resolve tasks. In their meta-analysis, Maillet and Rajah (2014)
881
noted that the regions that are over-recruited by older adults during successful encoding all overlap with or occur
882
in close proximity to regions that have been associated with encoding failures in young adults. In a recent study,
883
when performing a Stroop-like task (i.e., identifying number magnitude and physical size), Huang et al. (2012)
884
observed that the left posterior parietal cortex (PPC) and right parietal cortex are recruited in young subjects
885
asked to identify number magnitude, while the right and left PPC were both recruited when these subjects were
886
asked to judge physical size, supporting the existence of compensatory processes in normal aging (see also
887
Nielson et al., 2002). These observations suggest that the HAROLD model may apply to regions other than the
888
PFC (Collins and Mohr, 2013).
889
The research has largely focused on the lateral parietal region, as damage to this region impairs some
890
aspects of EM(e.g., Davidson et al., 2008). The lateral parietal region may be activated during encoding and
891
retrieval (e.g., Ciaramelli et al., 2008), depending on the utilized material and studied sub-region, but it seems to
892
be more strongly associated with successful retrieval than successful encoding (for review, see Olson and
893
Berryhill, 2008). The encoding and retrieval of EM information requires some level of attention (e.g., Anderson
894
and Craik, 1974; Carrasco et al., 2004; Fernandes and Moscovitch, 2000; Moscovitch, 1992), which may depend
895
in part on the parietal cortex. Cabeza et al. (2008) proposed an anatomical model of memory and attention (the
896
Attention to Memory model), in which retrieval depends on distinct regions of the lateral PPC (Cabeza et al.,
897
2011;Naghavi and Nyberg, 2005; Spaniol, 2009). Indeed, parietal damage can impair the conscious retrieval of
898
even well encoded information (Bisiach and Luzzatti, 1978). The dorsal PPC region directs attention towards a
899
retrieval goal, whereas ventral PPC regions are implicated in bottom-up attention, as captured by environmental
900
stimuli or sensory cues. Distinctions can also be made between the superior and inferior parietal regions, which
901
show complementary patterns of activity: the superior area appears to reflect top-down influence in mediating
902
low-confidence responses, while the inferior region reflects a bottom-up influence that mediates high-confidence
903
responses (Kim and Cabeza, 2007). Studies have shown that different parietal regions are differentially involved
904
in various processes related to retrieval (Vilberg and Rugg, 2008). In fMRI studies using the R/K paradigm,
905
parietal activations were found to be stronger for items accompanied by vivid, clear recollections compared to
906
those accompanied by a feeling of knowing (Henson et al., 1999; Skinner and Fernandes, 2007; Wheeler and,
907
2004; for review, see Wagner et al., 2005). The dorsal parietal cortex is believed to support familiarity, whereas
24
908
the ventral region is concerned with recollection. Within the cortex, the temporo-parietal region contributes to
909
recollection, while the occipito-parietal region is associated with familiarity (Daselaar et al., 2006).
910
Another structure that has been highlighted as playing a role across a range of cognitive functions
911
(including EM) is the cerebellar region. The effects of aging on this structure are less well understood, however,
912
as no study has yet compared its activation between young and old people. Schacter et al. (1996) proposed that
913
(similar to the PFC) the cerebellum might be involved in strategic processes, retrieval efforts and the inhibition
914
of irrelevant information. Andreasen et al.(1995) underlined the close anatomical connections between the
915
cerebellum and the PFC, and suggested that (similar to the left PFC) the right cerebellum might belong to a
916
general memory circuit involved in the encoding of information. However, the data are inconsistent across
917
studies. Cerebellar activations were reported only for verbal materials and showed a tendency for right
918
lateralization during encoding tasks in some studies (Cabeza and Nyberg, 2000; Fliessbach et al., 2007), while
919
others have found that activation of the cerebellum appears to favor retrieval over encoding, and to
920
predominantly concern the left cerebellar hemisphere (Desgranges et al., 1998; Wiggs et al., 1999). Further
921
studies are needed to elucidate any age-related differences and to understand the specific role of the
922
cerebellum.The MRI- and PET-based study of age-related structural and functional changes performed by
923
Desgranges et al. (2008) showed that the most highly deteriorated morphological structures include the frontal
924
and parietal cortices, and the more caudal aspect of the hippocampal regions. The best-preserved regions, in
925
contrast, include the rostral hippocampal regions and the thalamus, especially the lateral nuclei. At the functional
926
level, the frontal and parietal cortices are the most sensitive to the effects of aging, followed by the MTL, while
927
the other regions are preserved. These results are consistent with the developmental hypothesis, which states that
928
the brain regions that develop first are the most resistant to the effects of aging, whereas the regions that develop
929
last are the most fragile.
930
While the above-described overview of the main involved anatomical structures provides insight into
931
their declines in normal aging, an emerging (yet consistent) finding in memory research is there are also age-
932
related differences in the functional connectivities of brain regions. Close anatomical linkages between the
933
parietal, occipital, frontal and medial temporal lobes have been shown to support EM encoding and retrieval
934
(Olson and Berryhill, 2009). During EM, age differences have been observed in studies that measured brain
935
activity during the successful encoding of words (Dennis and Cabeza, 2008), scenes (St Jacques et al., 2009) and
936
objects (Addis et al., 2010) with the Dm effect paradigm. During successful encoding, the elderly have a weaker
937
functional connectivity between the MTL and posterior regions (i.e., the occipital or parietal cortices), but
938
greater connectivity between the MTL and PFC, as compared to younger adults (Daselaar et al., 2006; Dennis et
939
al., 2008; Hayes et al., 2008; Leshikar et al., 2010; Park & McDonough, 2013). Some authors have found age-
940
related reductions in the fronto-temporal network during memory encoding (Grady et al., 1995; Grady et al.,
941
2003; Wang et al., 2010;), while altered fronto-occipital connectivity has also been observed with increasing age
942
(Moeller et al., 1996). Cabeza et al. (2004) found that older adults showed decreases in parietal and occipital
943
regions coupled with increases in PFC regions. Age-related differences in functional connectivity have also been
944
found during retrieval, most notably in temporal-parietal connectivity during recognition tasks. Using a verbal
945
task, Daselaar et al. (2006) demonstrated that older adults had reduced frontal connectivity within a
946
hippocampal–parietotemporal network relative to young adults, but increased connectivity within a
947
parahippocampal–frontal network. This result was interpreted as indicating that older adults compensate for
948
hippocampal deficits by relying more on the parahippocampal cortex. This is consistent with the notion that
25
949
older adults globally compensate for decreases in the neuronal activity of one brain region by recruiting
950
additional resources to perform a cognitive task (Dennis and Peterson, 2012; Davis et al., 2008).
951
In conclusion, EM is assembled in a complex circuit. Neurocognitive models of EM postulate that the
952
strategic component of the observed deficit depends primarily on the PFC, whereas the associative component
953
mostly relies on the MTL, especially the hippocampus (e.g., Simons and Spiers, 2003; Shing et al., 2010 for
954
reviews; Shing and Lindenberger, 2012). Along with the parietal cortex, these are key structures in both
955
encoding (Rombouts et al., 1997; Stern et al., 1996) and retrieval (e.g., Shannon and Buckner, 2004; Dennis and
956
Cabeza, 2008) of EM. Although little explored, EM deficits in older adults can also be related to age-related
957
differenceswithin the same group, between individuals, and according to single or multiple factors. Those same
958
factors might also be responsible for the accelerated declines seen in the most important neurodegenerative
959
diseases (i.e., AD), and may help direct the onset of the symptoms and the intra-individual differences that can
960
be seen between two people at the same stage of the disease.
961
5/ Inter-individual variability associated with EM in normal aging and Alzheimer disease
962
5.1/ Lifestyle
963
Age affects EM performance among healthy individuals (Kramer et al., 2003), but there are clearinter-
964
individual variabilities (Christensen et al., 1999; Morris and Price, 2001; Raz et al., 2009): while some people
965
decline rapidly and experience severe memory impairment at a relatively young age, even to the point of being
966
diagnosed with dementia, others undergo“normal” or even “successful” aging with little change (or even some
967
improvement)in their mental capacity into extreme old age (Albert et al., 1995; Dixon and de Frias, 2014; Reed
968
et al., 2010; Rubin et al., 1998; Wilson et al., 2002; Zelinski et al., 1993).When cognitive capacities decline in
969
aging, and particularly AD, EM is one of the first systems to fail (Hodges, 2000). Longitudinal studies have
970
confirmed that individual differences in cognitive performance increase from early to late adulthood (e.g., de
971
Frias et al., 2007); a number of individual characteristics have been found to be critically associatedwith the
972
variances in this process, and thusmay contribute to modulating the effects of aging on cognitive functions
973
(Anstey and Christensen 2000; Lemaire and Bherer, 2005). Two major negative factors are obesity
974
(e.g.,Sellbomand Gunstad, 2012) and hypertension (e.g.,Etgen et al., 2010; Raz and Rodrigue,2006; see also
975
Deary et al., 2009), and environmental and genetic influences also appear to be involved (e.g., Deary et al.,
976
2009;Finkel et al., 2005; McGue et al., 1993).Colombes et al. (2006) and Stern (2002) showed that the negative
977
effects of aging could be slowed throughout life (including in centenarians)bythe protective effects derived from
978
continuous cognitive stimulation, whichcontributesto thecognitive reserve (CR).In addition,heritability studies
979
have indicated that genetic variants strongly influence differences in cognitive ability throughout the lifespan,
980
including in old age (e.g., Tupler et al., 2007; Mormino, 2014)
981
The concept ofreserve (both passive and cognitive), which provides a framework for explaining
982
individual-level characteristics (Stern, 2011), reflects the amount of damage that can be sustained before
983
reaching a critical threshold at which clinical signs manifest (Bastin et al., 2013; Brickman et al., 2011;
984
Kalpouzos et al., 2008; Nyberg et al., 2012; Satz, 1993).The passive reserve refers to differences in brain
985
structure, such as neuronal density (Villeneuve and Belleville, 2010), which may increase the brain’s tolerance
986
of disease. This brain reserve differs from the CR, which Stern (2002, 2009) defined as an individual’s ability to
26
987
optimize or maximize performance on cognitive tasks by recruiting the same or different (neural compensation)
988
brain networkscompared to young subjects, and thus using alternative cognitive strategies (Baldivia et al., 2008).
989
The CR hypothesis posits that at any given level of clinical severity, the underlying pathology of AD is more
990
advanced in patients with a higher level of CR (Vemuri et al., 2011). IQ (e.g.,Christensen et al., 2007; Willerman
991
et al., 1991), social interactions (e.g., Fritsch et al., 2007; Scarmeas and Stern, 2003), leisure activities [both
992
cognitive (Fratiglioni et al., 2004; Fritsch et al., 2007; Stern, 2006) and physical (Anstey and Christensen, 2000;
993
Nithianantharajah and Hannan, 2009; Smith et al., 2014)], level of education (Andel et al., 2006; Bruandet et al.,
994
2008; Christensen et al., 2009; Fritsch et al., 2002; Singh-Manoux et al., 2011; Vance et al., 2010),and
995
professional activities (e.g., Andel et al., 2006; Fritsch et al., 2002)confera lifelong set of skills that maylengthen
996
an individual’s resistance against age-related cognitive declines and reduce his or her risk of
997
developingAlzheimer’s disease(for review, see alsoScarmeas and Stern, 2003; Valenzuela and Sachdev, 2006).
998
Alzheimer's patients with a high CR but a more advanced disease stagecan operate at a level of clinical severity
999
equivalent to that of lower CR patients in earlier stages of the disease.However, such patients show greater AD-
1000
related brain damage (i.e., parieto-temporal and frontal hypoperfusion)andonce the cognitive decline begins in
1001
such individuals, it progresses more quickly than in other groups (Hall et al., 2007; Figure 3). Scarmeas et al.
1002
(2004) demonstrated that the hippocampus plays an important role in the reservesof AD patients, assignificant
1003
activation of this structure seems to be the optimal response in AD patients with high CR.
1004 1005 1006
- Insert Figure 3 about here –
1007 1008
1009
5.2/ Genetics
1010
Although lifestyle factors can help people grow older successfully, new research has also focused on the
1011
roles played by genetic differences, especially given that EM is a heritable and polygenic trait
1012
(Papassotiropoulos and de Quervain, 2011). In normal populations(Plomin et al., 2001; Plomin and Spinath,
1013
2002; Friedman et al., 2008), including twin and adoption studies (Bouchard and McGue, 1981; Bouchard and
1014
McGue, 2003; Carmelli et al., 1997; Petrill et al., 2001), over 50% of the variance in adult cognitive ability is
1015
thought to arise from genetic influences. In recent years, researchers have linked specific genes (COMT, BDNF,
1016
ApoE4 for the main) to cognitive functioning and EM in older adults (Goldberg and Weinberger, 2004; Harris
1017
and Deary, 2011), as well as many of the dementias that have been seen in older populations.
1018
As a variety of evidence has implicated the PFC and dopaminergic pathways in cognition and EM (e.g.,
1019
Dickinson and Elvevag, 2009; for review,see Lisman and Grace, 2005; Shohamy and Adcock, 2010), some
1020
researchers have focused on genes that are related to the regulation of dopaminergic function. Evidence suggests
1021
that the relationship between DA levels and prefrontal cognitive performance follows an inverted-U-shaped
1022
function, where performance is impaired by the presence of too little or too much DA (Mattay et al., 2003; for
1023
review, see Cools andD’Esposito, 2011).Catechol-O-methyl transferase (COMT) is an enzyme that inactivates
1024
the release of DA (Raz et al., 2009). Humans havea functional polymorphism in the COMT gene, where a
27
1025
methionine (Met) for valine (Val) substitution at codon 158 (Val158Met) reduces the enzyme’s thermostability
1026
and activity (Chen et al., 2004; Lewis et al., 2001; Mazei et al., 2002; Moron et al., 2002), thereby decreasing the
1027
degradation of DA in the neocortex. The high-activity Val allele, in contrast, directs faster catabolism of
1028
prefrontal DA at the synapse, impairing prefrontal function and reducing performance on a range of cognitive
1029
tasks among Val carriers compared to non-Val carriers (e.g., Egan et al., 2001). COMT has been mainly
1030
associated with executive functions in studies of both younger and elderly individuals (Payton, 2009), with
1031
homozygotes for the low-activity Met allele performing better than subjects with the high-activity Val allele
1032
(Malhotra et al., 2002; for review, see also Greenwood andParasuraman, 2003). De Frias et al. (2004) found an
1033
association of this functional polymorphism with EM, with Met/Met carriers outperforming the Val carriers, as
1034
found by Bates et al. (2003) on a delayed visual memory-recall task (see also Savitz et al., 2006 for a
1035
review).However, a meta-analysis yielded mixed results, including little to no association between the COMT-
1036
Val158Met genotype and cognitive function (Barnett et al., 2008).
1037
The gene encoding brain-derived neurotrophic factor (BDNF) has been associated with EM
1038
performance (de Quervain et al., 2003; Egan et al., 2003; Ho et al., 2006; Voineskos et al., 2011; see also
1039
Papassotiropoulos and de Quervain, 2011 but see Harris et al., 2006; Dennis et al., 2011; Laing et al., 2012;
1040
Gong et al., 2012 for inconsistent findings) and appears to play a role in the MTL, primarily in the hippocampus
1041
(Greenwood andParasuraman, 2003; Hariri et al., 2003; Kambeitz et al., 2012), but also in the PFC (Bertolino et
1042
al., 2006; Pezawas et al., 2004) in humans and non-human species. A steady decline in BDNF expression has
1043
been associated with normal aging (Tapia-Arancibia et al., 2008), while in AD,its expression is reduced in the
1044
hippocampus and entorhinal cortex (i.e., the first structures to be pathologically degraded).This neurotrophin has
1045
been linked to the long-term potentiation-mediated facilitation of memory formation (Poo, 2001). A common
1046
functional Val-to-Met substitution at amino acid 66 (Val66Met) has been identified, with the Met allele
1047
associated in some studies with impaired BDNF trafficking and poorer EM performance (e.g., Hariri et al., 2003;
1048
Kambeitz et al., 2012), while other studies reported contradictory results (Harris and Deary, 2011; Dennis et al.,
1049
2011). Nevertheless, behavioral results from Egan et al. (2003) showed that the BDNF polymorphism is
1050
associated with delayed recall of stories but not word lists, suggesting a different involvement according on the
1051
task. Furthermore, Met carriers appeared to exhibit poorer performance (Koppel and Goldberg, 2009) and
1052
reduced neural activity within the MTL when performing EM tasks(Bath and Lee, 2006; Bueller et al., 2006;
1053
Hairi et al., 2003;Kauppi et al., 2014). The Met BDNF allele is associated withabnormal hippocampal function
1054
and greater prefrontal activity (Mattay et al., 2008). This may reflect the presence of a compensatory mechanism
1055
that can maintain performance and decreased EM performances in elderly subjects and young healthy
1056
individuals compared to BDNF Val homozygotes (Pezawas et al., 2004).Voineskos et al. (2011) showed that
1057
elderlyVal homozygoteswere characterized by decreases in EM performance, entorhinal cortex thickness,
1058
andintegrity of the white matter tract. Additionally, functional brain imaging studies indicated that Met carriers
1059
exhibit higher MTL activity than non-Met carriers during both encoding and retrieval ofEM tasks (Dennis et al.,
1060
2011), even when the analysis controlled for cognitive performance. The authors suggested that this increased
1061
activity might be needed to match the memory performance of non-carriers. The possible interaction ofthe
1062
COMT and BDNF polymorphisms has been examined. For example, Miller and Cohen (2001) proposed that the
1063
two factors might jointly regulate the prefrontal-MTL circuit responsible for EM,while Nagel et al. (2008) found
1064
an interaction between BDNF Val66Met, COMT Val158Met, and age. The latter authors posited that older
1065
individuals homozygous for the Val allele of COMT experienced additional performance declines if they were
1066
also BDNF Met-carriers, suggesting that the BDNF polymorphism negatively modulates the interaction between
28
1067
age and Val-COMT. Moreover, Witte et al. (2012) reported that the interaction between these COMT and BDNF
1068
polymorphisms explained significantly more of the variation in cortical plasticity than either gene alone.
1069
Finally, a functional polymorphism in the gene that encodes apolipoprotein (ApoE) is the most clearly
1070
established genetic risk factor for AD (for review, see Grady, 2012). ApoE is a ubiquitous protein that plays a
1071
major role in the clearance of beta-amyloid (A), which is thought to be the neurotoxic agent of AD. The
1072
encoding gene has three allelic variations in the human population:2, 3, and 4. In contrast to 2 and 3
1073
carriers, 4 allele carriers are at adose-dependently increasedrisk for developing AD (Havlik et al., 2000;
1074
Katzman et al., 1997; Moffat et al., 2000; Perry et al., 2001), with two copies of 4 increasing the risk of
1075
developing early AD to 80%, compared toa risk of 20% in the absence of the allele (Corder et al., 1993; for
1076
ameta-analysis, see Farrer et al., 1997). Compared to the heterozygous carriers, 4 homozygotes have greater
1077
deficits in EM tasks (e.g., Nilsson et al., 2006; Matura et al., 2014), even when such individuals are selected as
1078
“high functioning” (Bretsky et al., 2003); they also show reduced bilateral MTL volumes (Lemaître et al.,
1079
2005).However, 4-carrier status is associated with greater longitudinal declines in memory performance, which
1080
become evident by the sixth decade of life (Caselli et al., 2009). A recent study by Kantarci et al. (2012) showed
1081
for the first time that the ApoE genotype modifies the association between cognition and the A load, which is
1082
measured with PIB-Pittsburgh compound B andconstitutes the senile plaques in cognitively normal older adults
1083
(see also Sparks et al., 1996). While PIB retention was modestly associated with cognitive function even after
1084
the data were adjusted for age, sex, and education, the presence of the ApoE 4 allele significantly increased the
1085
A load and influenced the relationship between the A load and cognitive function, increasing the risk of
1086
cognitive decline in healthy individuals. Another tracer (18F-FDDNP) was used by Shoghi-Jadid et al. (2002) to
1087
label bothNFT(Neurofibrillary tangles) and A deposits, the main proteins that misfold and accumulate in AD.
1088
The authors found significant accumulation of this marker in the hippocampal region, a strong link between
1089
marker fixation areas and hypometabolism areas,and a negative correlation between marker accumulation and
1090
EM. Kauppi and colleagues (2014) recently investigated the combined effect of APOE and BDNF on
1091
hippocampal activity and found thatthe APOE 4 and BDNF Met alleles were associated with decreased
1092
activation of the anterior (hippocampus) and posterior (parahippocampal gyrus) parts of the MTL(see also Ward,
1093
2014; conversely, see Richter-Schmidinger et al., 2011). Faster EM declines and reduced hippocampal
1094
volumeswere found in Met carriersof BDNF with high A loads among those in the prodromal stage of AD (Lim
1095
et al., 2014). However, it is important to emphasize that the ApoE 4 allele appears to have only a limited effect
1096
on cognition in dementia-free individuals (e.g., Small et al., 2000). In a recent study, Ferencz et al. (2013) did
1097
not find that ApoE alone affected hippocampal (HC) volume and EM performance in adults older than 60
1098
years;however, they did observe an association between HC volume and free recall performance in ApoE 4
1099
carriers who also carried the risk alleles of TOMM40, which encodes a protein that is required for transporting
1100
proteinsinto mitochondria. On a functional level, PET studies revealed widespread reductions in the glucose
1101
metabolism of cognitively intact adults (50-65 years old) (Reiman et al., 1996),and in younger adults carrying
1102
the 4 allele (20-39 years old, Reiman et al., 2004), as assessed in the posterior cingulate, temporo-parietal and
1103
prefrontal regions (i.e., the same regions that exhibit metabolic deficits in AD patients) (Alexander et al., 2002).
1104
These observations suggest that the neural networks that sub-serve EM function are altered in APOE 4 carriers
1105
in a manner similar to that observed in subjects with early dementia (i.e., MCI; Bookheimer et al., 2000).
1106
Additionally, healthy ApoE 4 carriers show volume reductions in the hippocampus (Cohen et al., 2001; Moffat
29
1107
et al., 2000), the white matter (Plassman et al., 1997) and the gray matter in the medial temporal and fronto-
1108
temporal regions (Wishart et al., 2006), compared to non-carriers. However, a study by Han and colleagues
1109
(2007) found that multiple right hemisphere brain regions were activated more strongly during a verbal paired-
1110
associated learning task in ApoE 4 non-demented older adults compared to their non-4 counterparts. The
1111
authors suggested that at-risk personsmight require additional structures to maintain a level of behavioral
1112
performance equivalent to that of non-4 allele carriers.
1113
In sum, the existence of a large inter-individual variation in performance and neuronal substrate has often
1114
been reported in the literature and this variability even seems to increase with age. Several characteristics appear
1115
critical in the appearance of these interindividual differences, including environmental, genetic and “self”
1116
(education, activities…) factors. The emotional state of the subjects and the congruence of this state at the time
1117
of encoding and recall might also influence this variability (Syssau, 1998 for review). With the existence of these
1118
risk factors, how EM decline is seen in Alzheimer disease?
1119
6/ Episodic memory and Alzheimer disease
1120
6.1/ Pathophysiology and characteristics of the disease
1121
AD is a progressive, irreversible and severely disabling disorder of memory and cognition that inevitably
1122
results in the need for intensive care, and ultimately indeath. Initially discovered by Aloïs Alzheimer in 1906,
1123
AD is a neurodegenerative disease of the central nervous system. The disease is characterized by two types of
1124
microscopic brain lesions, amyloid plaques (or senile plaques; Gouras et al., 2000) and neurofibrillary tangles
1125
(NFT; Grundke-Iqbal et al., 1986), along with neuronal and synaptic loss. Amyloid plaques arise from the
1126
extracellular accumulation of Aß protein (a metabolic waste product), whileNFTreflect accumulation of the tau
1127
protein, which is inactivated by hyper-phosphorylation and found as conglomerates in the cell body of the
1128
neuron and its extensions. The microscopic lesions lead to neuronal dysfunction and death, yielding the
1129
macroscopic result of altered brain activity and cortical atrophy, with the brain losing about 8-10% of its weight
1130
within a decade. In vivo neuroimaging techniques (i.e., MRI and PET) have revealed that this atrophy first
1131
develops in the MTL, entorhinal cortex and hippocampus (Schwindt and Black, 2009), andthen spreads into the
1132
neocortex (Delacourte et al., 1999), followed by thesubcortical nuclei, brainstem and cerebellum (Thal et al.,
1133
2002).
1134
In the absence of any clear biological or neurological marker, AD is also characterized by cognitive deficits
1135
that gradually affect overall cognitive functioning. Of the five major memory systems, most authors consider the
1136
EM system to be the most clinically relevant for AD patients (e.g.,Bäckman et al., 2004; Dubois et al., 2007;
1137
McKhann, 2011;Small and Bäckman, 2007; Thomas-Anterion and Laurent, 2006),given that impairments in this
1138
system can worsen memory for recent events, leading to functional deficits. AD has a preclinical period called
1139
MCI (Mild Cognitive Impairment), during which early and mild cognitive deficits can be identified (e.g., Bordet
1140
et al., 2010); in 50% of affected individuals, this period evolves to AD pathology within a few years
1141
(Trojanowski et al., 2010). Although MCI may therefore represent a prodromal stageof AD, it is a heterogeneous
1142
syndrome, with some patients never progressing to dementia (Richard and Brayne, 2014).
30
1143
6.2/ Behavioral data
1144
Patients with AD show deficits in EM from the very early stages of the disease. These performance deficits
1145
reflect disorders of encoding andstorage (e.g., Pena-Casanova et al., 2012) but also retrieval. These disorders are
1146
often associated with temporal and spatial disorientation, and patients often have difficulties withEM tasks (for
1147
review, see Ergis& Eusop-Roussel, 2008). In memory consultations for the early detection of dementia, one of
1148
the most widely used tests for assessing EM is called “free recall-cued recall 16 items” (Desgranges and
1149
Eustache, 2003).This test aims to differentiate EM pure disorders from apparent memory deficits. Whereas pure
1150
memory disorders are due to problems with encoding or consolidation, underpinned by the hippocampus,
1151
apparent memory deficits are related to the use of inefficient strategies, attentional disorders that affect memory
1152
performance, and information-retrieval disorders, underpinned by the frontal cortex (Eustache et al., 2006).This
1153
verbal test, developed by Grober and Buschke (1987) is based on the encoding depth (the subject is asked to
1154
perform semantic processing of presented words) and encoding specificity (the same clues are used during
1155
encoding and recovery, and the effectiveness of retrieval cues depends on the conditions under which the
1156
information was encoded). In AD, the obtained pattern largely favors an encoding disorder, with AD patients
1157
having difficulties with establishing an elaborate (deep semantic) encoding of either the target information or the
1158
context (e.g., Bird and Luszcz, 1991; Bondi and Kaszniak, 1991; Monti et al., 1996) compared to healthy older
1159
people. Moreover, AD patients have performance deficits in both recall and recognition, leading some
1160
researchers to posit the presence ofan encoding deficit (Delis et al., 1991; Bäckman and Small, 1998). Dalla
1161
Barda and Goldblum (1996)found that the recognition performances of their non-healthy participantswere lower
1162
than those of the control group, and patients were less capable of correctly associating items by their semantic
1163
relationships (see also Goldblum et al., 1998). Similar to AD patients, MCI subjects gain little benefit from the
1164
semantic links that would normally be used during the encoding of words (Perri et al., 2005). This difficulty
1165
could reflect either an inability to discriminate between two related concepts due to loss of the details
1166
distinguishing the concepts (e.g., Martin and Fedio, 1983; Sailor et al., 1998) or an inability to relate those
1167
concepts during encoding. Moreover, some authors have observed that patients are unable to retrieve information
1168
when the recall task is delayed (e.g., Hart et al., 1988), suggesting that there is a deficit in the consolidation of
1169
information during the formation ofEM. This lack of storage would mostly appear in free recall tests rather than
1170
cued recall or recognition tasks (Christensen et al., 1998).
1171
Considerable data support the hypothesis that the weak EM performance of Alzheimer's patients might
1172
come from a deficit at the retrieval level of information, which appears to arise in the early stages of the disease
1173
(Perri et al., 2007) and leads affected individuals to forget quickly (Delis et al., 1991). AD patients typically have
1174
difficulties learning lists of words; moreover, once a list is learned, they quickly have difficulty recalling the
1175
words or recognizing them among distractors (Delis et al., 1991; Moulin et al., 2004; Traykov et al., 2007). As
1176
seen for encoding, patients benefit little from semantic cueing or environmental support, and their sensitivity to
1177
indicesdecreases as the disease progresses (Ergis and Eusop-Roussel, 2008; Libon et al., 1996; Wagner et al.,
1178
2012). They also appear to be unable to inhibit irrelevant associations (Helkala et al., 1989). However,
1179
contradictions appear:some studies have noted performance deficits for both recognition and free recall
1180
(Bäckman et al., 2001; Delis et al., 1991), while others found normal performance for recognition, at least during
1181
the first stage of the disease (e.g., Karlson et al., 2003; Tounsi et al., 1999). In some cases, free recall was found
1182
to be less successful in patients (e.g., Bartok et al., 1997; Kramer et al., 1988), and although the superior recall of
1183
pictures (compared to words) is preserved in AD patients (Ally et al., 2009), some authors found similar
31
1184
performances between recall and recognition tasks using both verbal and pictorial items (e.g., Deweer et al.,
1185
1993;Eslinger and Damasio, 1986; Fleischman et al., 1997; Grosse et al., 1990; Heindel et al.,1988; Koivisto et
1186
al., 1996;Greene et al., 1996). These findings suggest that the EM deficit observed among AD patients reflects
1187
an issue with learning rather than an acceleration of forgetting or disruption of retrieval. Tounsi et al. (1999)
1188
used the RL/RI 16 items test to examine 131 AD patients divided into four sub-groups according to the severity
1189
of dementia (i.e., pre-clinical to severe). Using a cued recall task, the authors showed that performance worsened
1190
withdisease progression, suggesting that retrieval is disordered at an early stage of AD. Retrieval deficits are also
1191
observed for autobiographical memory in patients with moderate stage of the disease, with consequences for
1192
future thinking. They are able to remember the past and imaging the future. However, patients will generate
1193
future events that are closely linked with their past memories, as few amount of memories are available (El haj et
1194
al., 2015a, 2015b). This inability to detach from the little information kept in memory to create new ones might,
1195
according to the authors, comes from a decline of flexibility, underpinned by the frontal lobes as well as from an
1196
alteration of the hippocampus.
1197
Piolino et al. (2003) demonstrated that familiarity processes are preserved in AD, whereasdeteriorations
1198
are seen in the controlled processes of conscious recollection. This conclusion is in line with the findings of
1199
Balota et al. (2002), who used a word recognition task in which they manipulated the frequency oftarget items
1200
and lures, and reported thatADpatients showed diminished performance on low-frequency words but not high-
1201
frequency words, as the latter triggered familiarity processes through their high frequency in the language.
1202
Conversely, lures were well rejected regardless of their degree of familiarity. Comparable results have been
1203
reported in MCI patients, with authors noting altered recollection but preservation of familiarity processes
1204
(Anderson et al., 2008; Hudon et al., 2009; Westerberg et al., 2006). Thus, it seems that recollection processes
1205
(i.e., those that allow subjects to retrieve items and their encoding context)may be sensitive right from the
1206
prodromal stage of AD,whereas familiarity processes are less sensitive. However, the deficits in encoding and
1207
consolidation increase as the pathology progresses,suggesting that rather thanbeing a sole deficit inretrieval, the
1208
desired information fails to be properly encoded.
1209
AD patients exhibit great difficulty in evoking memories and information, and also suffer from memory
1210
distortions (Balota et al., 2002; Budson et al., 2000; Dalla Barbaet al., 1999). Traditionally, studies in the field
1211
have focused on analyzing the negative symptoms that characterize the memory disorders related to Alzheimer's
1212
disease. More recently, however, researchers have turned to theso-called “positive” symptoms, such as extra-list
1213
intrusions, whichare the production of words that do not belong to the presented list in a recall task, and false
1214
recognition, which occurs when a subject is convinced that he or she recognizes an item even though it was not
1215
previously presented in the recognition task (Adam, 2006). Desgranges et al. (2002) suggested that different
1216
intrusions may arise via different processes: free recall intrusions that lack any semantic link to the target words
1217
may be attributed to deficits in strategic processes, reflecting a frontal dysfunction, whereas cued recall
1218
intrusions are induced relatively automatically by indices, reflecting rhinal dysfunction (Ergis and Eusop-
1219
Roussel, 2008). Several studies showed that ADpatients had a generally positive response bias (i.e., a tendency
1220
to always say “yes, I have seen this item”) in recognition tests (Pillon et al., 1993; Snodgrass andCorwin, 1988).
1221
Balota et al. (2002) used the mirror effect paradigm to account for this phenomenon. Subjects first memorize a
1222
series of words(50% with low lexical frequency, 50% high lexical frequency), and then are exposed to a
1223
distracting task before being testedwith a yes/no recognition task. The mirror effect paradigm predicts that low-
1224
frequency wordswill trigger more correct recognitions and less false recognition relative to items with a high
1225
lexical frequency. In AD, however, the opposite is observed. Budson et al. (2000), and Balota et al. (1999)
32
1226
showed that,compared to controls, Alzheimer's patientscommit fewer false recognitions after a single exposure
1227
to a list of semantically associated items, but show higher levels of false recognition after repeated exposure to
1228
the same list. This suggests that Alzheimer patients build up a semantic gist across trials, whereas controls
1229
distinguishacross all semantic items (i.e., if “tulip” is in list 1, “daisy” is in list 2 and “lily” is in list 3, controls
1230
will remember the semantic category of “flower” but not each individual item).
1231
6.3/ Neural structures implicated inEM declines
1232
The age-related decline in EMis a continuous process (Sexton, 2010) that arises from the dysfunction of an
1233
integrated network and (at least in AD) involves specific pathologies of both gray and white matter. Patients with
1234
a neurodegenerative disease, at least in the early stages of disease evolution, may present with very
1235
circumscribed neurocognitive impairment, as confirmed by the use of brain imaging. For example, Desgranges
1236
et al. (1998) used PET and a “cognitive-metabolic correlation” strategy to show that specific damages to
1237
different memory systems are related to specific and highly focused abnormalities in brain metabolism.However,
1238
impaired EM seems to be linked to dysfunction of an extensive network that includes the hippocampus and PFC
1239
(dorsal and ventral medial PFC, bilaterally), along with other regions, such as the posterior
1240
cingulate/retrosplenial cortex, the precuneus, the inferior parietal lobule and the hippocampal formation (i.e.
1241
entorhinal cortex and parahippocampal cortex) (Greicius et al., 2003; Laird et al., 2009). These structures are
1242
also known to be involved in the so-called default mode network(DMN; Eustache et al., 2006; Buckner et al.,
1243
2008 for reviews).The DMN, participating in EM (e.g. Shapira-Lichter et al., 2013), is an interconnected and
1244
anatomically defined brain system that preferentially activates in states of relative rest but deactivate during
1245
external-orienting tasks (e.g. Anticevic et al., 2012 ; Buckner et al., 2008). Deactivation of key nodes of the
1246
DMN, in coordination with hippocampal activation, may in fact be a prerequisite for successful memory
1247
encoding (Daselaar and Cabeza, 2004 ; Miller et al., 2008). Conversely, there is evidence that failure to suppress
1248
activity in some of the core default mode areas such as the precuneus is associated with failed encoding and poor
1249
performance in subsequent memory tests in cognitively normal young and old subjects (e.g. Otten and Rugg,
1250
2001)Several authors found a concordance between AD-related atrophy and healthy intrinsic functional
1251
connectivity in the DMN (Buckner et al., 2005; Greicius et al., 2004, Seeley et al., 2009).In recent fMRI studies
1252
of AD, corresponding brain default mode regions have been found to demonstrate an abnormal fMRI task-
1253
induced deactivation response pattern.Deactivation is progressively disrupted from normal aging to MCI and to
1254
clinical AD (Philajamaki and Sperling, 2009). In other words, the weaker the deactivations become in the DMN,
1255
the greater risk to develop the disease is important (e.g. Petrella et al., 2007). Moreover, the functionnal
1256
disconnection between the posterior cingulate cortex and the hippocampus may explain some of their EM
1257
impairments (e.g. Chételat et al., 2003 ; Villain et al., 2008).
1258
Most studies agree that the AD pathologybegins with the formation of NFT in the MTL. As the severity of
1259
the disease increases, the NFTprogressively accumulates and structural atrophy increases (Duyckaerts et al.,
1260
1998; Delacourte et al., 1999). In the early to moderate stages of AD, EM formation is critically underpinned by
1261
the hippocampal region (Baron et al., 2001; Desgranges, 2008) and the entorhinal cortex (Scheltens et al., 2002;
1262
for review, see Braak et al., 1999; Chételat and Baron, 2003; Taylor and Probst, 2008; see also Hirni et al.,
1263
2013). The temporo-parietal and posterior cingulate cortices are also affected, and the disease spreads to other
1264
neocortical regionsas the severity increases (Atienza et al., 2011; Gomez-Isla et al., 1996). In vivo imaging
1265
studies have shown that certain regions (e.g., the posterior parietal, cingulate and retrosplenial cortices) contain
33
1266
exceptionally high levels of amyloid plaques in AD patients, andamyloid deposition in the parietal cortex
1267
isnegatively correlated with glucose metabolism, suggesting that activity is diminished in this region (Klunk et
1268
al., 2004). As shown by Wolk et al. (2011), the neural substrates required to integrate and process information
1269
vary significantly depending on the stage of processing (i.e., encoding and/or retrieval).
1270
Functional disturbances of resting metabolism in AD brains have also been observed in a pattern
1271
mimicking structural modifications. A number of studies have reported either similar (Heun et al., 2007;
1272
Sandström et al., 2006) or increased MTL and notably increased hippocampal activity (Fleisher et al., 2005) in
1273
at-risk persons (i.e.,MCI patients orasymptomatic carriers of at least one ApoEɛ4 allele) compared to controls
1274
during EM tasks.However, hypometabolism and hypoperfusion of the temporo-parietal and posterior cingulate
1275
cortices constitute the earliest and most frequent dysfunction in AD(e.g.,Grön et al., 2004; Lind et al.,
1276
2006;Loessner et al. 1995) and are associated with pure EM disorders (e.g.,Desgranges and Eustache, 2005;
1277
Bäckman et al., 1999; Golby et al., 2005; Gron et al., 2002; Pariente et al., 2005). Asymmetry of the temporo-
1278
parietal cortex is reported in most PET studies of affected individuals with right hemispheric alterations noted in
1279
patients with MCI (Chételat et al., 2003; Mosconi et al., 2004) or moderate AD (Nagahama et al., 2003; for
1280
review, see Chételat et al., 2006). The reported results are somewhat heterogeneous, which can be explained in
1281
part by differences in the utilized methodologies and studied disease stages. For example, Desgranges et al.
1282
(2002) compared groups of patients at different stages of AD in an effort to follow the organization of brain
1283
networks during the course of the disease. EM was measured by PET analysis during retrieval, using a story
1284
recall test in a group of 40 patients divided into two subgroups (n=20 patients per group)based on their Mini
1285
Mental State Examination (MMSE) scores.For those having the highest MMSEscores (i.e. MCI), the significant
1286
correlationswere restricted to limbic structures, including the hippocampal, parahippocampal/perirhinal,
1287
entorhinal and retrosplenial cortices. This finding suggests that the dysfunction of these regions is responsible for
1288
the first declines in EM seen among AD patients. In the more severe subgroup, whichincluded patients with
1289
more profound pathology-associated memory deficits,correlations with EMwere found with regions of the
1290
neocortex, particularly the temporal lobe, which has been implicated in semantic memory. These correlations
1291
have been interpreted as reflecting a compensatory mechanism that is activated by the disease (for review, see
1292
Eustache et al., 2006). Compared to elderly controls, patients with mild AD show hypoactivations of MTL when
1293
encoding scenes or pictures (Machulda et al., 2003; Rombouts et al., 2000; Small et al., 1999), recognizing
1294
geometric patterns (Gron et al., 2002), and retrieving associations (Dickerson et al., 2005; Pariente et al., 2005;
1295
Sperling et al., 2003). In most studies, additional activations are seen in various neocortical regions, particularly
1296
the frontal (and also parietal) region, in patients with established AD (e.g.,Bäckman et al., 1999; Grady et al.,
1297
1993; Grossman et al., 2003; Rémy et al., 2005; Yetkin et al., 2006),and in MCI patients during EM tasks (Heun
1298
et al., 2007). During encoding and retrieval, patients showed consistently greater activity in the right DL-PFC
1299
and left or bilateral VL-PFC when compared to controls. The observed PFC differences between patients and
1300
elderly controls were unidirectional, with AD patients showing greater PFC activity than controls. A relationship
1301
between VL-PFC and the MTL has been documented, in that the degree of activity in the left VL-PFC is greater
1302
in older adults with less MTL activity during encoding (Gutchess et al., 2005). The same phenomenon has been
1303
observed in the medial parietal cortex and posterior cingulate gyrus(Sperling et al., 2003, Fouquet et al.,
1304
2007).Although overactivation might support improved performance in the short term, it could also be a sign that
1305
an individual is compensating for a progressive pathology (and therefore could predict future declines).
1306
In recent years there has been an emphasis in exploring the dynamic properties of the subregions (dentate
1307
gyrus, Ammon’s horn, subiculum) of the hippocampus rather than examining the hippocampus as a
34
1308
homogeneous structure. Indeed, subfields of the hippocampus are not uniformly affected by the disease. The
1309
function of the dentate gyrus (DG) is manifold but it has a key role in the processing of spatial information and
1310
memory processes : formation of new memories (Zhao et al., 2008), associative memory (Morris, 2006), spatial
1311
pattern separation (Kesner, 2013), context pattern separation (Lee and Solivan, 2010 ; Wei Deng et al., 2013) for
1312
some of its main role. The human dentate gyrus have the unique property of persistent adult neurogenesis (Li et
1313
al., 2008). It is thought to play an important role in hippocampus-dependent learning and memory. Li and
1314
colleagues found that, in AD, although neuroproliferation increase, the differentiation of newly born cells into
1315
mature neurons is compromised. However, the dentate gyrus has been shown to withstands neurodegenerative
1316
disease markers until late stage of AD (Ohm, 2007). This is also true for the CA3 region, part of the ammon’s
1317
horn (Gómez-Isla et al.,1996). On the contrary, the CA1 zone is vulnerable to the disease as an atrophy, neuronal
1318
loss and NFT are observed (Mueller et al., 2010 ; Pluta et al., 2012, West, 1994). The anatomy suggests that the
1319
subiculum might participate in multiple reverberating circuits linking the hippocampus and the wider temporal
1320
cortex. It would compare novel stimuli from the entorhinal cortex with temporarily stored information in the
1321
hippocampus (Witter et al., 2000). The subiculum might also receive multiple mapped versions of the same
1322
space possibly facilitating the construction of distinct spatial maps (Menendez, 2006). Although mildly affected
1323
in early stages, significant reductions in the amount of dendrites (i.e. neural number) have been shown in AD,
1324
particularly in later stages (Rossler et al., 2002 ; West, 1994).
1325
Finally, although the cerebellum is not considered to be a primary focus of AD pathology, differences have
1326
been noted in cerebellar regions upon both encoding and retrieval. Indeed, while the cerebellum was traditionally
1327
thought to be unaffected in AD, neuropathological studies haveidentified cerebellar changes in the late stage of
1328
the disease (Rapoport et al., 2000; Wegiel et al., 1998). One study revealed that patients showed very large
1329
activationsof the left and right cerebellar hemispheres upon encoding (however, this work failed to specify the
1330
disease stage)(Schwindt and Black, 2009). Ishii et al. (1997) found that cerebellar metabolism was decreased in
1331
severe AD, and this decrease was correlated with the MMSE score. Together, these results suggest that atrophy
1332
progresses with the severity of AD, spreading from the MTL to the entire cortex.
1333
In sum, EM impairment is reached very early in AD patients and differ according to the severity of the
1334
disease. These performance deficits reflect specific disorders to one or more of the steps of encoding, storage
1335
and/or recovery, but also the creation of false memories, such as the production of intrusion and false
1336
recognition.The pattern of EM impairments displayed by AD patients is consistent with damage to areas of the
1337
MTL (the entorhinal cortex being affected first) and frontal lobes. MRI findings have also suggested that the
1338
fornix and mammillary bodies are atrophied in AD compared with healthy controls and with patients with MCI.
35
1339
7/ Conclusion and perspectives
1340
Over the last few years, neuroimaging studies (fMRI and PET) conducted on EMhave revealed that
1341
different brain networks are involved in healthy elderly subjects or AD patients compared to the reference
1342
population (i.e., young subjects). However, the study of EM has not been limited to PET- and fMRI-based
1343
methodologies,and numerous researchers have used other techniques, such asevent-related potentials(ERPs) or
1344
transcranial magnetic stimulation(TMS), to explore the responses of thebrain. The age-related decline in EM has
1345
been associated with structural and functional alterations in the PFC, the MTL (including the hippocampus and
1346
parahippocampal regions), the parietal lobe, the cingulate gyrus, and the cerebellum. Such studies have further
1347
suggested that different mechanisms may be involved in age-related versus pathology-related memory
1348
impairments.
1349
In normal aging, changes in the PFC (the most sensitive structure) seem to underlie the age-related
1350
declines in memory performance, at least among the oldest subjects. The central role of this structure is also
1351
emphasized by the finding that its activity increases in response to the under-recruitment of the MTL, reflecting
1352
a compensatory mechanism (for an example, see Gutchess et al., 2005). EM difficulties also appear to be linked
1353
to more general declines in attentional, executive and speed processing, which are further associated with
1354
volume reductions in the frontal cortex. From a behavioral point of view, Craik and Jennings (1992) noted that
1355
age effects are difficult to characterize in terms of a single dimension, instead appearing to represent a complex
1356
interaction between participants, materials, and variables of encoding and retrieval. The existence of a cognitive
1357
reserve, although difficult to measure, could also explain the apparent discrepancies between the results of
1358
different studies.
1359
Understanding the age-associated deficits in memory is important for two reasons. First, in view of the
1360
growing number of older adults in today’s society, cognitive aging is increasingly becoming a problem of
1361
general health care, and effective therapeutic intervention methods can only be developed on the basis of
1362
knowledge obtained through fundamental research. Second, there is a subgroup of elderly with more severe
1363
memory impairments that prevent them from functioning normally within their environment. Such memory
1364
impairments can be the earliest manifestation of pathological age-related conditions, such as AD. Particularly in
1365
the early stages of the disease, it is difficult to distinguish the AD pathology (i.e., EM impairments) from normal
1366
age-related memory impairments. In the first stages of the disease (i.e., MCI), the entorhinal cortex and its
1367
associated structures in the anterior MTL are affected (Hirni et al., 2013). The AD lesions progress to the parietal
1368
cortex and neocortex,and then affect the frontal lobe. Thus, the brain areas that sub-serve residual EM shift from
1369
the limbic to the neocortical structures as the AD-related cognitive impairment becomes more severe. Deficits in
1370
EM are already present in patients with MCI, potentiallyreflecting the first symptoms of disease.Thus, even if
1371
activities of daily living are preserved, EM impairments could constitute an important early marker that
1372
neurologists might use to identify individuals at higher risk for developing AD.
1373
Going forward, the challenge will be to further advance our understanding of the biological and
1374
psychological aspects of memory in normal aging, such that specific lifestyle changes (e.g., an exercise regimen
1375
and dietary supplements) and pharmacological treatments can be recommended to middle-aged and older adults,
1376
in the hopes of supporting satisfactory memory performance and relatively independent living well into the ninth
1377
and tenth decades of life. Successful treatments would presumably be those that increase the recruitment of
36
1378
additional neural networks to support declining networks whose functions have become inefficient and/or noisy.
1379
This may arise through the multiple mechanisms of neural plasticity that continue to function in older adulthood.
1380
37
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Figure 1: Classification of the different memory systems: short-term and working memory systems versus the
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long-term storage systems (inspired by Tulving, 1995).
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Figure 2: The three processes of episodic memory and their neural substrates. Abbreviations: MTL, medial
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temporal lobe; and mPFC, medial and lateral prefrontal cortices.
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Figure 3: Progression of Alzheimer’s disease (AD) according to the amount of cognitive reserve (CR; high or
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low). The stars indicate the critical threshold of brain damage, beyond which the clinical signs of AD are seen
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