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Cognitive reserve: A catalyst for research
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Abstracts / Journal of the Neurological Sciences 283 (2009) 240–320
Therapy with statins in AD has not yet proven significance in improving the disease and its progress. However, the use of peripherally acting statins is recommended due to the fact that by reducing plasma CH, peripheral hypercholesterolemia is avoided. doi:10.1016/j.jns.2009.02.067
Cerebral hypoperfusion and clinical onset of dementia
M. Breteler Erasmus University Medical Center, Rotterdam, The Netherlands Background: Cerebral blood flow (CBF) is decreased in Alzheimer patients. The question is whether this reflects diminished demand due to advanced neurodegeneration or that cerebral hypoperfusion contributes to dementia, possibly through vascular brain damage and consequential white matter lesions (WML). Methods: Within the Rotterdam Study, a prospective population based study of persons aged 55 years and over, we examined the relation of CBF velocity as measured with transcranial Doppler with dementia and markers of incipient dementia (i.e. cognitive decline and hippocampal and amygdalar atrophy on MRI). Moreover, we investigated how CBF as measured with 2Dphase-contrast MRI (both absolute (in ml/min) and adjusted for brain volume (brain tissue perfusion, in ml/min/100 ml brain tissue) relates to WML volume and to cognitive function. Results: Persons with higher CBF velocity were less likely to have dementia. Furthermore, in non-demented persons, higher CBF velocity was related to significantly less cognitive decline over the preceding period and larger hippocampal and amygdalar volumes. Persons with a low CBF performed worse on tests of global cognitive function and information processing speed, but had similar volume of WML, when compared with persons with high CBF. However, when taking brain atrophy into account, CBF was no longer associated with cognitive function, but lower brain tissue perfusion was associated with significantly more WML. Conclusions: A low CBF velocity is associated with dementia, but also with markers of incipient dementia. Brain tissue perfusion is not related to cognitive function crosssectionally, but persons with low brain tissue perfusion have more WML. Although we cannot exclude that preclinical neurodegeneration leads to hypoperfusion, our data suggest that cerebral hypoperfusion precedes and contributes to the onset of clinical dementia, possibly by contributing to WM pathogenesis. doi:10.1016/j.jns.2009.02.068
Cognitive reserve: A catalyst for research
Y. Stern Columbia University, New York, NY, USA The concept of cognitive reserve suggests that the differences in how individuals process tasks can provide a reserve against brain pathology, or age-related changes. Epidemiologic studies have found that individuals with greater cognitive reserve—as indicated by higher IQ, education, occupational attainment or participation in leisure activities—experience slower age-related cognitive decline and a reduced risk for Alzheimer's disease and other dementias. Imaging studies have begun to identify the neural basis for cognitive reserve, an important consideration in the early detection and treatment of dementia. Enhancing cognitive reserve may therefore help forestall age-related changes in the brain and the clinical onset of this disease. The concept of cognitive reserve also has direct implications for the diagnosis and treatment of any condition that affects brain function. doi:10.1016/j.jns.2009.02.069
Cognitive reserve in non-Alzheimer's dementias
R. Perneczkya, J. Diehl-Schmida, C. Pohla, P. Haussermannc, H. Boeckerd, A. Drzezgab, A. Kurza a Department of Psychiatry and Psychotherapy, Technical University Munich School of Medicine, Munich, Germany b Department of Nuclear Medicine, Technical University Munich School of Medicine, Munich, Germany c Centre For Integrative Psychiatry, Kiel, Germany d Department of Radiology, Rheinische Friedrich-Wilhelms-Universität Bonn, Bonn, Germany Background/aims: Previous studies suggest that cognitive reserve allows patients with a higher school education to cope better with brain damage. However, research has been focused on Alzheimer's disease (AD), and no studies existed so far exploring the cognitive reserve hypothesis in other neurodegenerative disorders. The aim of the present studies was therefore to provide evidence for cognitive reserve in neurodegenerative disorders other than AD, such as frontotemporal dementia (FTD), nonfluent progressive aphasia (NFPA), and dementia with Lewy bodies (DLB). Methods: 29 patients with FTD, 11 patients with NFPA, and 21 patients with DLB were included. Participants underwent a thorough diagnostic assessment including cerebral 18F-FDG-PET imaging. Regression analyses with the relative glucose metabolism as the dependent and years of schooling as the independent variables were conducted in SPM2 software. The global cognitive performance, as measured by a total score of the CERAD neuropsychological battery, was entered as confound in the statistical analyses in order to identify brain regions where patients with more years of school education had a lower relative metabolism at the same level of cognitive impairment. Results: There was a significant negative association between the relative glucose metabolism and the years of schooling in each patient group. The significant clusters were located in brain regions typically affected by the particular disorder, i.e. the bilateral inferior frontal cortex in the FTD group; the left inferior temporal, parahippocampal, and supramarginal gyri in the NFPA group; and the left temporo-parieto-occipital cortex in the DLB group. Conclusions: Our studies showed that more functional brain damage was necessary in patients with a higher school education to express the symptoms of their disease to a similar degree than patients with less schooling. We therefore suggest that cognitive reserve also helps patients with other neurodegenerative disorders than AD to attenuate the symptoms of progressive brain damage. doi:10.1016/j.jns.2009.02.070
HDDD with Alzheimer's disease as common comorbidity: A clinicopathologic case report R.M. Liscica,g, M.I. Behrensa,e,f, J.C. Morrisa,b,c,d, N.J. Cairnsa,b,c,d a Alzheimer's Disease Research Center, Zagreb, Croatia b Department of Pathology, Zagreb, Croatia c Immunology, Zagreb, Croatia d Neurology, Washington University School of Medicine, St. Louis, MO, USA e Departamento De Neurologia Y Neurochirurgia, Hospital Clinico Universidad De Chile, Santiago, Chile f Clinica Alemana, Santiago, Chile g Institute For Medical Research and Occupational Health, Zagreb, Croatia Background and aims: Hereditary dysphasic disinhibition dementia (HDDD) [1] describes a familial disorder characterized by personality changes, language and memory deficits. The neuropathology includes frontotemporal lobar atrophy, neuronal loss and gliosis and, in most cases abundant amyloid beta (Aß) plaques and neurofibrillary tangles (NFTs). A Pick/Alzheimer's spectrum was proposed for the original family HDDD1. Here we report the clinicopathologic case of an HDDD1 individual with additional Alzheimer's disease (AD) pathology, as a common comorbidity, which may mislead clinicians in diagnosis. Methods: Modern immunohistochemical methods; DNA sequencing. Results: Clinical onset was at age 62 years with personality changes and disinhibition, followed by non-fluent dysphasia, and dementia (characterized by memory deficits and spatial disorientation), that progressed to muteness with death at the age of 84. There was severe generalized brain atrophy (weight = 570 g). Histopathology showed superficial microvacuolation,
Abstracts / Journal of the Neurological Sciences 283 (2009) 240–320
Therapy with statins in AD has not yet proven significance in improving the disease and its progress. However, the use of peripherally acting statins is recommended due to the fact that by reducing plasma CH, peripheral hypercholesterolemia is avoided. doi:10.1016/j.jns.2009.02.067
Cerebral hypoperfusion and clinical onset of dementia
M. Breteler Erasmus University Medical Center, Rotterdam, The Netherlands Background: Cerebral blood flow (CBF) is decreased in Alzheimer patients. The question is whether this reflects diminished demand due to advanced neurodegeneration or that cerebral hypoperfusion contributes to dementia, possibly through vascular brain damage and consequential white matter lesions (WML). Methods: Within the Rotterdam Study, a prospective population based study of persons aged 55 years and over, we examined the relation of CBF velocity as measured with transcranial Doppler with dementia and markers of incipient dementia (i.e. cognitive decline and hippocampal and amygdalar atrophy on MRI). Moreover, we investigated how CBF as measured with 2Dphase-contrast MRI (both absolute (in ml/min) and adjusted for brain volume (brain tissue perfusion, in ml/min/100 ml brain tissue) relates to WML volume and to cognitive function. Results: Persons with higher CBF velocity were less likely to have dementia. Furthermore, in non-demented persons, higher CBF velocity was related to significantly less cognitive decline over the preceding period and larger hippocampal and amygdalar volumes. Persons with a low CBF performed worse on tests of global cognitive function and information processing speed, but had similar volume of WML, when compared with persons with high CBF. However, when taking brain atrophy into account, CBF was no longer associated with cognitive function, but lower brain tissue perfusion was associated with significantly more WML. Conclusions: A low CBF velocity is associated with dementia, but also with markers of incipient dementia. Brain tissue perfusion is not related to cognitive function crosssectionally, but persons with low brain tissue perfusion have more WML. Although we cannot exclude that preclinical neurodegeneration leads to hypoperfusion, our data suggest that cerebral hypoperfusion precedes and contributes to the onset of clinical dementia, possibly by contributing to WM pathogenesis. doi:10.1016/j.jns.2009.02.068
Cognitive reserve: A catalyst for research
Y. Stern Columbia University, New York, NY, USA The concept of cognitive reserve suggests that the differences in how individuals process tasks can provide a reserve against brain pathology, or age-related changes. Epidemiologic studies have found that individuals with greater cognitive reserve—as indicated by higher IQ, education, occupational attainment or participation in leisure activities—experience slower age-related cognitive decline and a reduced risk for Alzheimer's disease and other dementias. Imaging studies have begun to identify the neural basis for cognitive reserve, an important consideration in the early detection and treatment of dementia. Enhancing cognitive reserve may therefore help forestall age-related changes in the brain and the clinical onset of this disease. The concept of cognitive reserve also has direct implications for the diagnosis and treatment of any condition that affects brain function. doi:10.1016/j.jns.2009.02.069
Cognitive reserve in non-Alzheimer's dementias
R. Perneczkya, J. Diehl-Schmida, C. Pohla, P. Haussermannc, H. Boeckerd, A. Drzezgab, A. Kurza a Department of Psychiatry and Psychotherapy, Technical University Munich School of Medicine, Munich, Germany b Department of Nuclear Medicine, Technical University Munich School of Medicine, Munich, Germany c Centre For Integrative Psychiatry, Kiel, Germany d Department of Radiology, Rheinische Friedrich-Wilhelms-Universität Bonn, Bonn, Germany Background/aims: Previous studies suggest that cognitive reserve allows patients with a higher school education to cope better with brain damage. However, research has been focused on Alzheimer's disease (AD), and no studies existed so far exploring the cognitive reserve hypothesis in other neurodegenerative disorders. The aim of the present studies was therefore to provide evidence for cognitive reserve in neurodegenerative disorders other than AD, such as frontotemporal dementia (FTD), nonfluent progressive aphasia (NFPA), and dementia with Lewy bodies (DLB). Methods: 29 patients with FTD, 11 patients with NFPA, and 21 patients with DLB were included. Participants underwent a thorough diagnostic assessment including cerebral 18F-FDG-PET imaging. Regression analyses with the relative glucose metabolism as the dependent and years of schooling as the independent variables were conducted in SPM2 software. The global cognitive performance, as measured by a total score of the CERAD neuropsychological battery, was entered as confound in the statistical analyses in order to identify brain regions where patients with more years of school education had a lower relative metabolism at the same level of cognitive impairment. Results: There was a significant negative association between the relative glucose metabolism and the years of schooling in each patient group. The significant clusters were located in brain regions typically affected by the particular disorder, i.e. the bilateral inferior frontal cortex in the FTD group; the left inferior temporal, parahippocampal, and supramarginal gyri in the NFPA group; and the left temporo-parieto-occipital cortex in the DLB group. Conclusions: Our studies showed that more functional brain damage was necessary in patients with a higher school education to express the symptoms of their disease to a similar degree than patients with less schooling. We therefore suggest that cognitive reserve also helps patients with other neurodegenerative disorders than AD to attenuate the symptoms of progressive brain damage. doi:10.1016/j.jns.2009.02.070
HDDD with Alzheimer's disease as common comorbidity: A clinicopathologic case report R.M. Liscica,g, M.I. Behrensa,e,f, J.C. Morrisa,b,c,d, N.J. Cairnsa,b,c,d a Alzheimer's Disease Research Center, Zagreb, Croatia b Department of Pathology, Zagreb, Croatia c Immunology, Zagreb, Croatia d Neurology, Washington University School of Medicine, St. Louis, MO, USA e Departamento De Neurologia Y Neurochirurgia, Hospital Clinico Universidad De Chile, Santiago, Chile f Clinica Alemana, Santiago, Chile g Institute For Medical Research and Occupational Health, Zagreb, Croatia Background and aims: Hereditary dysphasic disinhibition dementia (HDDD) [1] describes a familial disorder characterized by personality changes, language and memory deficits. The neuropathology includes frontotemporal lobar atrophy, neuronal loss and gliosis and, in most cases abundant amyloid beta (Aß) plaques and neurofibrillary tangles (NFTs). A Pick/Alzheimer's spectrum was proposed for the original family HDDD1. Here we report the clinicopathologic case of an HDDD1 individual with additional Alzheimer's disease (AD) pathology, as a common comorbidity, which may mislead clinicians in diagnosis. Methods: Modern immunohistochemical methods; DNA sequencing. Results: Clinical onset was at age 62 years with personality changes and disinhibition, followed by non-fluent dysphasia, and dementia (characterized by memory deficits and spatial disorientation), that progressed to muteness with death at the age of 84. There was severe generalized brain atrophy (weight = 570 g). Histopathology showed superficial microvacuolation,