- Email: [email protected]
E-ADNI study: Preliminary data
Poster Presentations: P4
P805
minor role in primacy performance. Specific associations between hippocampus volume and delayed primacy performance as reported in cognitively healthy elderly may be masked by global memory impairment in aMCI.
P4-087
P4-086
IS HIPPOCAMPAL SIZE ASSOCIATED WITH PRIMACY RECALL PERFORMANCE IN AMNESTIC MILD COGNITIVE IMPAIRMENT?
uggen2, Michel J. Grothe2, Elisabeth Kasper1, Katharina Br€ Davide Bruno3, Nunzio Pomara4, Marco Duering5, Michael Ewers5, Katharina Buerger5, Stefan J. Teipel6,7, 1University of Rostock, Rostock, Germany; 2German Center for Neurodegenerative Diseases (DZNE), Rostock, Germany; 3Liverpool Hope University, Liverpool, United Kingdom; 4Nathan Kline Institute, Orangeburg, NY, USA; 5Institute for Stroke and Dementia Research, M€unchen, Germany; 6German Center for Neurodegenerative Disease (DZNE), Rostock, Germany; 7Department of Psychosomatics, University Medical Center Rostock, Rostock, Germany. Contact e-mail: [email protected] Background: Delayed recall of the first words of a word list - the primacy position – is supposed to be particularly dependent on intact memory consolidation and has been shown to predict general cognitive decline in elderly people (Bruno et al. 2013). A previous study suggested hippocampal volume loss to be the primary neuronal correlate of reduced delayed primacy recall in cognitively normal elderly individuals (Bruno et al. 2015). Here, we studied the association of hippocampus volume with immediate and delayed primacy recall in people with amnestic mild cognitive impairment (aMCI), and assessed the specificity of these effects compared with non-primacy recall. Methods: We investigated 88 subjects with aMCI. Serial position performance was tested using a 16-word list. Primacy (recall of first 4 words) and non-primacy performance (recall of words on positions 5 to 16) were measured for short and delayed recall. Hippocampal volumes were automatically determined from structural MRI scans. We conducted partial correlation analyses of bilateral hippocampus volumes and primacy and non-primacy indices controlling for age, total intracranial volume (TIV), and overall recall performance. Results: After controlling for age and TIV, bilateral hippocampal volume was significantly associated with immediate primacy recall, but not with delayed primacy recall. Furthermore, hippocampal volume was significantly associated with both short and delayed non-primacy recall. These effects, however, were no more significant after additionally controlling for overall recall performance. By contrast, overall delayed recall performance was significantly associated with hippocampal volume, even after controlling for primacy or non-primacy delayed recall. Conclusions: Our findings suggest that in conditions of progressive neurodegeneration, such as aMCI, the hippocampus might play only a
LONGITUDINAL WHITE MATTER ALTERATIONS OF MCI PATIENTS IN WP5 PHARMACOG/E-ADNI STUDY: PRELIMINARY DATA
Moira Marizzoni1, Jorge Jovicich2, Flavio Nobili3, Mira Didic4,5, David Bartres6, Ute Fiedler7, Peter Schonknecht8, Pierre Payoux9,10, Alberto Beltramello11, Andrea Soricelli12,13, Lucilla Parnetti14, Magda Tsolaki15, Paolo Maria Rossini16,17, Philip Scheltens18, Gianluigi Forloni19, Regis Bordet20, Olivier Blin21, Giovanni Battista Frisoni22,23 , PharmaCog Consortium, 1Laboratory of Epidemiology, Neuroimaging and Telemedicine/ IRCCS Istituto Centro San Giovanni di Dio Fatebenefratelli, Brescia, Italy; 2University of Trento, Trento, Italy; 3University of Genoa, Genoa, Italy; 4Service de Neurologie et Neuropsychologie, Marseille, France; 5Aix-Marseille Universite, Marseille, France; 6Universitat de Barcelona and IDIBAPS, Barcelona, Spain; 7 Institutes and Clinics of the University Duisburg-Essen, Essen, Germany; 8 Department of Neuroradiology, University Hospital Leipzig, Leipzig, Germany; 9Imagerie Cerebrale et Handicaps Neurologiques, Toulouse, France; 10Universite de Toulouse, Toulouse, France; 11General Hospital, Verona, Italy; 12IRCCS SDN, Naples, Italy; 13University of Naples Parthenope, Naples, Italy; 14University of Perugia, Perugia, Italy; 15 Aristotle University of Thessaloniki, Thessaloniki, Greece; 16Policlinic Gemelli, Rome, Italy; 17Catholic University of Rome, Rome, Italy; 18VU University Medical Center, Amsterdam, Netherlands; 19IRCCS Istituto di Ricerche Farmacologiche “Mario Negri”, Milano, Italy; 20University of Lille Nord de France, Lille, France; 21Aix-Marseille University-CNRS, Marseille, France; 22IRCCS Istituto Centro San Giovanni di Dio Fatebenefratelli, Brescia, Italy; 23Memory Clinic and LANVIE - Laboratory of Neuroimaging of Aging, University Hospitals and University of Geneva, Geneva, Switzerland. Contact e-mail: [email protected] Background: Workpackage5 of PharmaCog (E-ADNI) is a serial
multicenter European study aimed to identify new biomarkers of disease progression in 147 patients with amnestic mild cognitive impairment (aMCI). Aim of this study is to investigate the longitudinal effects of amyloid and neurodegeneration on the white matter alterations in these patients. Methods: We report preliminary diffusion longitudinal data of 78 aMCI patients who underwent CSF collection at baseline and high resolution 3T MRI at baseline and after 12 months. Patients were enrolled in 13 memory clinics in Italy, France, Spain, Germany, Greece and The Netherlands. An atlas-based DTI analysis was performed to collect measures of fractional anisotropy (FA), mean, axial and radial diffusivity (MD, AD and RD, respectively) from corpus callosum, superior and inferior lateral fasciculi and corticospinal tracts (Jovicich et al., 2014). Patients were divided into 4 groups based on their Ab42 and Ptau CSF levels: biomarker negative (Ab-Ptau-neg), amyloid positive only (Ab-pos), neurodegeneration positive only (Ptau-pos) and amyloid-neurodegeneration positive (Ab-Ptau-pos). General linear model for repeated measures was performed considering amyloid and neurodegenerative status as independent variables, diffusion estimates as dependent variables and age and gender as covariates. Post-hoc Tukey’s test was applied to compare the diffusion changes among the 4 groups. Results: After one year, a similar trend of alterations was observed for all the diffusion metrics considered:
P806
Poster Presentations: P4
Ab-Ptau-pos> Ptau-pos> Ab-pos> Ab-Ptau-neg. However, a significant interaction among time, Ab and PTau levels was reported only for RD (F(1,669)¼ 5.64, p¼ .02) and MD (F(1,669)¼ 7.01, p¼ .01). Ab-Ptau-pos showed higher increased in RD relative to aMCI without neurodegeneration (Ab-Ptau-neg and Ab-pos; Tukey’s test, p<.050) and higher MD increase compared to Ab-pos (Tukey’s test, p<.05). No significant FA and L1 alterations were observed. Conclusions: These preliminary data suggest that in aMCI patients i) amyloid pathology affects in white matter diffusion only when neurodegeneration coexists and ii) RD and MD seems more sensitive than FA and L1 to detect longitudinal diffusion changes. Longitudinal analysis is still ongoing. Pharmacog is funded by the EU-FP7 for the Innovative Medicine Initiative (grant 115009).
P4-088
LOWER CEREBRAL BLOOD FLOW IS ASSOCIATED WITH COGNITIVE DECLINE IN PATIENTS WITH ALZHEIMER’S DISEASE
Marije Benedictus, Annebet Leeuwis, Joost Kuijer, Philip Scheltens, Frederik Barkhof, M. Wiesje van der Flier, Niels Prins, VU University Medical Center, Amsterdam, Netherlands. Contact e-mail: m.benedictus@ vumc.nl Background: Cerebral blood flow (CBF) is lower in patient with Alzheimer’s disease (AD) compared to the general elderly population. We aimed to investigate whether lower CBF was associated with a more rapid cognitive decline in patients with AD. Methods: We included 88 AD patients from the Amsterdam dementia cohort, with an arterial spin labeling (ASL) scan at baseline and at least one year of clinical follow-up. 3T pseudocontinuous (PC-)ASL was used to determine whole brain and regional (parietal, frontal, occipital, temporal and cerebellar) CBF (ml/100gr/min). For statistical purposes, CBF was inverted
Table 1 Associations of CBF with baseline MMSE and annual change in MMSE Model 1 Cerebral blood flowx Whole brain Parietal Frontal Temporal Occipital Cerebellum
Estimated baseline MMSE -0.3260.39 -0.5060.41 -0.0260.43 -0.2060.39 -0.2960.38 0.2660.39
U
-0.50+0.25 -0.59+0.25* -0.1460.26 -0.4660.25 -0.47+0.25# -0.1860.26
Estimated baseline MMSE -0.2860.39 -0.45+0.41 0.1260.43 -0.17+0.39 -0.2360.39 0.3060.40
Estimated annual change in MMSE -0.49±10.25 -0.59±0.25* -0.1260.26 -0.4760.25 -0.47±0.25# -0.1760.26
P4-089
LOWER CEREBRAL BLOOD FLOW IS RELATED TO MORE SEVERE COGNITIVE IMPAIRMENT IN PATIENTS WITH DEMENTIA DUE TO ALZHEIMER’S DISEASE
Annebet Leeuwis1, Marije Benedictus1, Joost Kuijer1, Philip Scheltens1,2, Frederik Barkhof1,2, Niels Prins1, Wiesje M. van der Flier1,2, 1VU University Medical Center, Amsterdam, Netherlands; 2Neuroscience Campus Amsterdam, Amsterdam, Netherlands. Contact e-mail: [email protected] Table 1 Associations between CBF and cognitive domains in patients with mild cognitive impairment (MCI) and Alzheimer’s Disease (AD) Mild cognitive impairment
Model 2
Estimated annual change in MMSE
(i.e., higher is worse) and standardized. Linear mixed models were used to determine associations between CBF and cognitive decline over time as measured with the MMSE. We adjusted for age, sex, education and normalized brain volume, and in a separate model additionally for white matter hyperintensities and lacunes. Results: Patients were 6567 years old, 44 (50%) were female and mean baseline MMSE was 2264. Mean follow-up of 2.160.8 years and patients declined with -2.263.0 MMSE points per year. Linear mixed models revealed no associations between whole brain or regional CBF with baseline MMSE (table 1). One standard deviation (SD) lower whole brain CBF was associated with a steeper decline of 0.5 MMSE points per year (Model 1: b[SE] -0.50[0.25], p¼0.05). In particular, lower parietal CBF was associated with steeper annual decline on the MMSE (Model 1: b[SE] -0.59[0.25], p<0.05). Lower occipital CBF tended to be associated with cognitive decline as well (Model 1: b[SE] - 0.47[0.25], p¼0.06). Additional adjustment for white matter hyperintensities and lacunes did not change these results. CBF in frontal, temporal and cerebellar regions was not associated with cognitive decline. Conclusions: Lower CBF, in particular in the parietal lobes, is associated with a steeper decline on the MMSE. These findings indicate that CBF as measured with ASL may have value as prognostic marker for cognitive decline in patients with AD.
U
Data are represented as b6SE. Linear mixed models were used to investigate associations between CBF and change in MMSE. A random intercept and random slope for time (in years) were assumed. The model includes terms for the CBF measure, time, the interaction between the CBF measure and time and covariates. The given b in each first column represents the difference in baseline MMSE. In each second column, the b represents the difference in annual MMSE change. Negative values indicate that a lower CBF is associated with a decline in MMSE. Model 1: adjusted for age, sex, education and NBV. Model 2: additional adjustment for WMH and lacunes. *p< 0.05; Up¼0.05; #p¼0.06; x CBF was inverted (i.e., higher is worse) and given per SD deviation increase (worsening).
CBF
Global
Memory
Attention
Language
Visuospatial functioning
Whole brain Parietal Frontal Temporal Occipital Cerebellum
.10 .05 .12 .15 -.00 .12
.19 .15 .29** .20 .03 .14
.06 .07 .01 .04 .08 -.02
.09 .08 .09 .10 .02 -.03
.20 .16 .21 .12 .12 .12
.06 .02 .04 .02 .01 .02
Executive functioning .13 .17* .11 .16* .14* -.00
Executive functioning
Alzheimer’s disease
CBF
Global
Memory
Attention
Language
Visuospatial functioning
Whole brain Parietal Frontal Temporal Occipital Cerebellum
.11 .13 .11 .14 .08 -.01
.06 .10 .07 .08 .06 .00
.07 .08 .02 .06 .09 -.03
.20* .17* .20* .23** .16* .12
.13 .16 .02 .10 .26** .10
Data are represented as standardized beta coefficient. The given beta represents the association between CBF and the different cognitive domains. Cognition is expressed as a (composite) z-score. CBF: cerebral blood flow. Adjusted for age. gender and education, white matter hypenntensities. presence of lacunes and normalized brain volume. *p<0.05, **p<0.001.
P805
minor role in primacy performance. Specific associations between hippocampus volume and delayed primacy performance as reported in cognitively healthy elderly may be masked by global memory impairment in aMCI.
P4-087
P4-086
IS HIPPOCAMPAL SIZE ASSOCIATED WITH PRIMACY RECALL PERFORMANCE IN AMNESTIC MILD COGNITIVE IMPAIRMENT?
uggen2, Michel J. Grothe2, Elisabeth Kasper1, Katharina Br€ Davide Bruno3, Nunzio Pomara4, Marco Duering5, Michael Ewers5, Katharina Buerger5, Stefan J. Teipel6,7, 1University of Rostock, Rostock, Germany; 2German Center for Neurodegenerative Diseases (DZNE), Rostock, Germany; 3Liverpool Hope University, Liverpool, United Kingdom; 4Nathan Kline Institute, Orangeburg, NY, USA; 5Institute for Stroke and Dementia Research, M€unchen, Germany; 6German Center for Neurodegenerative Disease (DZNE), Rostock, Germany; 7Department of Psychosomatics, University Medical Center Rostock, Rostock, Germany. Contact e-mail: [email protected] Background: Delayed recall of the first words of a word list - the primacy position – is supposed to be particularly dependent on intact memory consolidation and has been shown to predict general cognitive decline in elderly people (Bruno et al. 2013). A previous study suggested hippocampal volume loss to be the primary neuronal correlate of reduced delayed primacy recall in cognitively normal elderly individuals (Bruno et al. 2015). Here, we studied the association of hippocampus volume with immediate and delayed primacy recall in people with amnestic mild cognitive impairment (aMCI), and assessed the specificity of these effects compared with non-primacy recall. Methods: We investigated 88 subjects with aMCI. Serial position performance was tested using a 16-word list. Primacy (recall of first 4 words) and non-primacy performance (recall of words on positions 5 to 16) were measured for short and delayed recall. Hippocampal volumes were automatically determined from structural MRI scans. We conducted partial correlation analyses of bilateral hippocampus volumes and primacy and non-primacy indices controlling for age, total intracranial volume (TIV), and overall recall performance. Results: After controlling for age and TIV, bilateral hippocampal volume was significantly associated with immediate primacy recall, but not with delayed primacy recall. Furthermore, hippocampal volume was significantly associated with both short and delayed non-primacy recall. These effects, however, were no more significant after additionally controlling for overall recall performance. By contrast, overall delayed recall performance was significantly associated with hippocampal volume, even after controlling for primacy or non-primacy delayed recall. Conclusions: Our findings suggest that in conditions of progressive neurodegeneration, such as aMCI, the hippocampus might play only a
LONGITUDINAL WHITE MATTER ALTERATIONS OF MCI PATIENTS IN WP5 PHARMACOG/E-ADNI STUDY: PRELIMINARY DATA
Moira Marizzoni1, Jorge Jovicich2, Flavio Nobili3, Mira Didic4,5, David Bartres6, Ute Fiedler7, Peter Schonknecht8, Pierre Payoux9,10, Alberto Beltramello11, Andrea Soricelli12,13, Lucilla Parnetti14, Magda Tsolaki15, Paolo Maria Rossini16,17, Philip Scheltens18, Gianluigi Forloni19, Regis Bordet20, Olivier Blin21, Giovanni Battista Frisoni22,23 , PharmaCog Consortium, 1Laboratory of Epidemiology, Neuroimaging and Telemedicine/ IRCCS Istituto Centro San Giovanni di Dio Fatebenefratelli, Brescia, Italy; 2University of Trento, Trento, Italy; 3University of Genoa, Genoa, Italy; 4Service de Neurologie et Neuropsychologie, Marseille, France; 5Aix-Marseille Universite, Marseille, France; 6Universitat de Barcelona and IDIBAPS, Barcelona, Spain; 7 Institutes and Clinics of the University Duisburg-Essen, Essen, Germany; 8 Department of Neuroradiology, University Hospital Leipzig, Leipzig, Germany; 9Imagerie Cerebrale et Handicaps Neurologiques, Toulouse, France; 10Universite de Toulouse, Toulouse, France; 11General Hospital, Verona, Italy; 12IRCCS SDN, Naples, Italy; 13University of Naples Parthenope, Naples, Italy; 14University of Perugia, Perugia, Italy; 15 Aristotle University of Thessaloniki, Thessaloniki, Greece; 16Policlinic Gemelli, Rome, Italy; 17Catholic University of Rome, Rome, Italy; 18VU University Medical Center, Amsterdam, Netherlands; 19IRCCS Istituto di Ricerche Farmacologiche “Mario Negri”, Milano, Italy; 20University of Lille Nord de France, Lille, France; 21Aix-Marseille University-CNRS, Marseille, France; 22IRCCS Istituto Centro San Giovanni di Dio Fatebenefratelli, Brescia, Italy; 23Memory Clinic and LANVIE - Laboratory of Neuroimaging of Aging, University Hospitals and University of Geneva, Geneva, Switzerland. Contact e-mail: [email protected] Background: Workpackage5 of PharmaCog (E-ADNI) is a serial
multicenter European study aimed to identify new biomarkers of disease progression in 147 patients with amnestic mild cognitive impairment (aMCI). Aim of this study is to investigate the longitudinal effects of amyloid and neurodegeneration on the white matter alterations in these patients. Methods: We report preliminary diffusion longitudinal data of 78 aMCI patients who underwent CSF collection at baseline and high resolution 3T MRI at baseline and after 12 months. Patients were enrolled in 13 memory clinics in Italy, France, Spain, Germany, Greece and The Netherlands. An atlas-based DTI analysis was performed to collect measures of fractional anisotropy (FA), mean, axial and radial diffusivity (MD, AD and RD, respectively) from corpus callosum, superior and inferior lateral fasciculi and corticospinal tracts (Jovicich et al., 2014). Patients were divided into 4 groups based on their Ab42 and Ptau CSF levels: biomarker negative (Ab-Ptau-neg), amyloid positive only (Ab-pos), neurodegeneration positive only (Ptau-pos) and amyloid-neurodegeneration positive (Ab-Ptau-pos). General linear model for repeated measures was performed considering amyloid and neurodegenerative status as independent variables, diffusion estimates as dependent variables and age and gender as covariates. Post-hoc Tukey’s test was applied to compare the diffusion changes among the 4 groups. Results: After one year, a similar trend of alterations was observed for all the diffusion metrics considered:
P806
Poster Presentations: P4
Ab-Ptau-pos> Ptau-pos> Ab-pos> Ab-Ptau-neg. However, a significant interaction among time, Ab and PTau levels was reported only for RD (F(1,669)¼ 5.64, p¼ .02) and MD (F(1,669)¼ 7.01, p¼ .01). Ab-Ptau-pos showed higher increased in RD relative to aMCI without neurodegeneration (Ab-Ptau-neg and Ab-pos; Tukey’s test, p<.050) and higher MD increase compared to Ab-pos (Tukey’s test, p<.05). No significant FA and L1 alterations were observed. Conclusions: These preliminary data suggest that in aMCI patients i) amyloid pathology affects in white matter diffusion only when neurodegeneration coexists and ii) RD and MD seems more sensitive than FA and L1 to detect longitudinal diffusion changes. Longitudinal analysis is still ongoing. Pharmacog is funded by the EU-FP7 for the Innovative Medicine Initiative (grant 115009).
P4-088
LOWER CEREBRAL BLOOD FLOW IS ASSOCIATED WITH COGNITIVE DECLINE IN PATIENTS WITH ALZHEIMER’S DISEASE
Marije Benedictus, Annebet Leeuwis, Joost Kuijer, Philip Scheltens, Frederik Barkhof, M. Wiesje van der Flier, Niels Prins, VU University Medical Center, Amsterdam, Netherlands. Contact e-mail: m.benedictus@ vumc.nl Background: Cerebral blood flow (CBF) is lower in patient with Alzheimer’s disease (AD) compared to the general elderly population. We aimed to investigate whether lower CBF was associated with a more rapid cognitive decline in patients with AD. Methods: We included 88 AD patients from the Amsterdam dementia cohort, with an arterial spin labeling (ASL) scan at baseline and at least one year of clinical follow-up. 3T pseudocontinuous (PC-)ASL was used to determine whole brain and regional (parietal, frontal, occipital, temporal and cerebellar) CBF (ml/100gr/min). For statistical purposes, CBF was inverted
Table 1 Associations of CBF with baseline MMSE and annual change in MMSE Model 1 Cerebral blood flowx Whole brain Parietal Frontal Temporal Occipital Cerebellum
Estimated baseline MMSE -0.3260.39 -0.5060.41 -0.0260.43 -0.2060.39 -0.2960.38 0.2660.39
U
-0.50+0.25 -0.59+0.25* -0.1460.26 -0.4660.25 -0.47+0.25# -0.1860.26
Estimated baseline MMSE -0.2860.39 -0.45+0.41 0.1260.43 -0.17+0.39 -0.2360.39 0.3060.40
Estimated annual change in MMSE -0.49±10.25 -0.59±0.25* -0.1260.26 -0.4760.25 -0.47±0.25# -0.1760.26
P4-089
LOWER CEREBRAL BLOOD FLOW IS RELATED TO MORE SEVERE COGNITIVE IMPAIRMENT IN PATIENTS WITH DEMENTIA DUE TO ALZHEIMER’S DISEASE
Annebet Leeuwis1, Marije Benedictus1, Joost Kuijer1, Philip Scheltens1,2, Frederik Barkhof1,2, Niels Prins1, Wiesje M. van der Flier1,2, 1VU University Medical Center, Amsterdam, Netherlands; 2Neuroscience Campus Amsterdam, Amsterdam, Netherlands. Contact e-mail: [email protected] Table 1 Associations between CBF and cognitive domains in patients with mild cognitive impairment (MCI) and Alzheimer’s Disease (AD) Mild cognitive impairment
Model 2
Estimated annual change in MMSE
(i.e., higher is worse) and standardized. Linear mixed models were used to determine associations between CBF and cognitive decline over time as measured with the MMSE. We adjusted for age, sex, education and normalized brain volume, and in a separate model additionally for white matter hyperintensities and lacunes. Results: Patients were 6567 years old, 44 (50%) were female and mean baseline MMSE was 2264. Mean follow-up of 2.160.8 years and patients declined with -2.263.0 MMSE points per year. Linear mixed models revealed no associations between whole brain or regional CBF with baseline MMSE (table 1). One standard deviation (SD) lower whole brain CBF was associated with a steeper decline of 0.5 MMSE points per year (Model 1: b[SE] -0.50[0.25], p¼0.05). In particular, lower parietal CBF was associated with steeper annual decline on the MMSE (Model 1: b[SE] -0.59[0.25], p<0.05). Lower occipital CBF tended to be associated with cognitive decline as well (Model 1: b[SE] - 0.47[0.25], p¼0.06). Additional adjustment for white matter hyperintensities and lacunes did not change these results. CBF in frontal, temporal and cerebellar regions was not associated with cognitive decline. Conclusions: Lower CBF, in particular in the parietal lobes, is associated with a steeper decline on the MMSE. These findings indicate that CBF as measured with ASL may have value as prognostic marker for cognitive decline in patients with AD.
U
Data are represented as b6SE. Linear mixed models were used to investigate associations between CBF and change in MMSE. A random intercept and random slope for time (in years) were assumed. The model includes terms for the CBF measure, time, the interaction between the CBF measure and time and covariates. The given b in each first column represents the difference in baseline MMSE. In each second column, the b represents the difference in annual MMSE change. Negative values indicate that a lower CBF is associated with a decline in MMSE. Model 1: adjusted for age, sex, education and NBV. Model 2: additional adjustment for WMH and lacunes. *p< 0.05; Up¼0.05; #p¼0.06; x CBF was inverted (i.e., higher is worse) and given per SD deviation increase (worsening).
CBF
Global
Memory
Attention
Language
Visuospatial functioning
Whole brain Parietal Frontal Temporal Occipital Cerebellum
.10 .05 .12 .15 -.00 .12
.19 .15 .29** .20 .03 .14
.06 .07 .01 .04 .08 -.02
.09 .08 .09 .10 .02 -.03
.20 .16 .21 .12 .12 .12
.06 .02 .04 .02 .01 .02
Executive functioning .13 .17* .11 .16* .14* -.00
Executive functioning
Alzheimer’s disease
CBF
Global
Memory
Attention
Language
Visuospatial functioning
Whole brain Parietal Frontal Temporal Occipital Cerebellum
.11 .13 .11 .14 .08 -.01
.06 .10 .07 .08 .06 .00
.07 .08 .02 .06 .09 -.03
.20* .17* .20* .23** .16* .12
.13 .16 .02 .10 .26** .10
Data are represented as standardized beta coefficient. The given beta represents the association between CBF and the different cognitive domains. Cognition is expressed as a (composite) z-score. CBF: cerebral blood flow. Adjusted for age. gender and education, white matter hypenntensities. presence of lacunes and normalized brain volume. *p<0.05, **p<0.001.