- Email: [email protected]
Association between brain amyloidosis, synaptic dysfunction and cognitive performance measured with ADAS-cog and MMSE scores in early MCI, late MCI and Alzheimer's disease
P48
Alzheimer’s Imaging Consortium Posters: IC-P
(Table 1). While decreased GMV in the prefrontal and temporal cortices, dorsal anterior cingulate, posterior cingulate and the insula were associated with the main effects of depression, increased GM atrophy in the thalamus, and default mode, executive control and medial temporal lobe (MTL) regions were related to the main effects of aMCI. Depression-aMCI interactive effects were associated with global GM volume loss involving cortical and MTL structures (P<0.05 FDR corrected; Figure 1). Depressive symptoms were negatively correlated and episodic memory performances were positively associated with GMV in similar brain regions as observed with LLD and aMCI respectively. Depressive symptom-memory deficit interactive effects were also seen globally, especially in the DMN and MTL regions. Conclusions: The interactive effects of LLD and aMCI are associated with GMV loss in crucial cognition and mood regulation structures. The co-existence of these clinical phenotypes may be a marker of AD.
IC-P-083
ASSOCIATION BETWEEN BRAIN AMYLOIDOSIS, SYNAPTIC DYSFUNCTION AND COGNITIVE PERFORMANCE MEASURED WITH ADAS-COG AND MMSE SCORES IN EARLY MCI, LATE MCI AND ALZHEIMER’S DISEASE
Marina Dauar1, Jared Rowley2, Liyong Wu3, Monica Shin3, Sara Mohades4, Vladimir Fonov5, Antoine Leuzy6, Serge Gauthier7, Pedro Rosa-Neto8, 1McGill Center for Studies in Aging, Montreal, Quebec, Canada; 2McGill University, Verdun, Quebec, Canada; 3McGill Center for Studies in Aging, Verdun, Quebec, Canada; 4McGill University, Verdun, Quebec, Canada; 5Montreal Neurological Institute, Montreal, Quebec, Canada; 6McGill Centre for Studies in Aging, Montreal, Quebec, Canada; 7 Alzheimer Disease Research Unit, McGill Center for Studies in Aging, Montreal, Quebec, Canada; 8McGill University, Montreal, Quebec, Canada. Background: Mini Mental Status Examination (MMSE) and Alzheimer’s Disease (ADx) Assessment Scale-cognitive subscale (ADAS-cog) are instruments for assessing cognitive deficits in ADx. Although MMSE and ADAS-cog differ in terms of complexity it is possible that both batteries convey comparable information regarding amyloid pathology or neurodegeneration. Here, we aimed to investigate the degree of association between two cognitive scales (ADAS-cog and MMSE), synaptic depletion and fibrillar amyloid deposition measured by [18F]FDG and [18F]AV45 PET, respectively. Methods: We analyzed a subsample of participants from the ADNIGO & ADNI2 who had clinical, neuropsychological, and [18 F] AV45/[18 F]FDG data collected in the course of a single visit. Diagnosis of cognitively normal (CN), early mild cognitive impairment (EMCI), late mild cognitive impairment (LMCI) and Alzheimer’s dementia (AD) was adjusted using ADNI2 guidelines. T1 MRIs underwent non-uniformity correction, were skull-stripped and nonlinearly registered to MNI152 space. After registration to MRI, PET uptake ratios (UR) were calculated by dividing [18 F]AV45 and [18 F]FDG scans by the median counts of cerebellar-gm and pons, respectively. PET images were subsequently registered to MNI152 space. Global [18 F]AV45 and [18 F]FDG estimates were conducted in
Table 1 Demographic information and behavioral performance CN (n ¼ 25) Mean Age (years) Education (years) Gender (F/M) MMSE DRS-2 raw scores Attention INIT/PERS Construct Conceptual Memory Total Paragraph Recall scores IMMED DELAYED HAMA GDS
Dep (n ¼ 18) SD
74.28 15.32
Mean
8.25 2.87
68.61 14.61
28.92
1.22
36.56 36.32 6.00 37.76 23.64 140.36 14.36 12.92 1.16 1.88
SD
aMCI (n ¼ 17)
aMCI/Dep (n ¼ 12)
Mean
Mean
SD
1.83
26.92
13.87 2.99 1.93c
0.043 0.175 0.135 0.001*
75.12 13.47
28.06
1.21
27.29
0.51 1.38 0.00 1.33 1.04 2.53
36.39 36.22 5.94 37.61 23.89 140.11
0.70 2.10 0.24 1.24 1.13 3.20
35.71 34.88 5.94 35.88 19.06 130.88
0.77b 3.62 0.24 2.45b 2.68b,d 5.49b,d
36.00 32.50 5.83 35.41 19.50 129.67
1.21 5.55 0.58 3.12c,e 3.60c,e 6.70c,e,f
0.004* 0.005 0.436 0.001* 0.000* 0.000*
3.73 4.03 1.06 2.11
14.17 12.06 10.88 17.28
3.96 4.24 5.07a 3.29a
8.41 2.47 2.18 4.35
3.59b,d 3.30b,d 1.55d 2.67d
7.17 3.25 8.67 14.25
3.76c,e 3.14c,e 4.19c,f 6.43c,f
0.000* 0.000* 0.000* 0.000*
14/4
68.33 14.25
P
6.81 2.57
12/13
6.62 2.07
SD
11/6
7/5
Notes. Significant differences (p<0.004, Bonferroni correction for multiple comparison) were found in MMSE, DRS-2 raw scores (except for INIT/PERS and Construct), Logical Memory II subscale (Immediate and Delayed Paragraph Recall) from the Wechsler Memory Scale – Revised and emotional scores (HAMA and GDS) among four groups. p values were obtained by one-way ANOVA analysis except for gender (X2 test). a-f: post-hoc analysis (Bonferroni correction) further revealed the source of ANOVA differences (a: CN vs Dep; b: CN vs aMCI; c: CN vs aMCI/Dep; d: Dep vs aMCI; e: Dep vs aMCI/Dep; f: aMCI vs aMCI/ Dep). Unless otherwise indicated, data are presented as mean 6 SD. Abbreviation: CN, cognitive normal; Dep, cognitively normal with late-life depression; aMCI, amnestic mild cognitive impairment; aMCI/Dep, amnestic mild cognitive impairment with late-life depression; M, mean; SD, standard deviation; F/M: female/male; MMSE, mini-mental state examination; DRS-2: dementia rating scale-2; INIT/PERS: Initiation/Preservation; IMMED, immediate recall scores; DELAYED, delayed recall scores; HAMA, Hamilton anxiety scales scores; GDS, geriatric depression scale scores.
Alzheimer’s Imaging Consortium Posters: IC-P
P49
Table 1 Demographic data, global uptake ratio of [18F]AV45 and [18F]FDG for all groups
Gender (M/F) Age (years) Education (years) MMSE CDR ADAS-cog Delayed recall of logical memory Global uptake ratio of AV45 Global uptake ratio of FDG
CN (n ¼ 109)
EMCI (n ¼ 157)
LMCI (n ¼ 39)
AD (n ¼ 49)
P value
53/56 78.8 6 5.9 16.4 6 2.8 29.1 6 1.2 060 6.2 6 4.2 14.0 6 3.7 1.28 6 0.25 1.29 6 0.13
90/67 73.1 6 7.9a 16.0 6 2.7 28.3 6 1.5a 0.5 6 0.1a 7.9 6 3.4a 9.3 6 2.1a 1.40 6 0.33a 1.31 6 0.15
24/15 76.2 6 9.2d 16.4 6 3.2 27.1 6 2.2 a,c 0.5 6 0.1a 12.5 6 5.7 a,c 3.5 6 2.8 a,c 1.56 6 0.36 a,c 1.22 6 0.15b,c
32/18 75.6 6 7.8d 16.7 6 2.8 21.4 6 4.7 a,c,e 1.0 6 0.4 a,c,e 21.8 6 10.3 a,c,e 1.5 6 2.6 a,c,e 1.62 6 0.38 a,c 1.14 6 0.15 a,c,e
0.231 <0.001 0.304 <0.001 <0.001 <0.001 <0.001 <0.001 <0.001
All values are indicated as mean 6 standard deviation except gender. p value indicates the value for the main effect of each group, as assessed with analyses of variance (ANOVA) for each variable except for gender, where a contingency chi-square was performed. Statistics for post hoc 2-by-2 group comparisons are provided as significant differences: a from CN at P<0.01; b from CN at P<0.05; c from EMCI at P<0.01; d from EMCI at P<0.05; e from LMCI at P<0.01. native space grey matter regions. Voxel-based age-corrected regression analysis was calculated from images resampled in MNI152. Results: Demographics are summarized in table 1. For all groups collapsed, [18 F] AV45-UR correlated with MMSE only in CN (temporal lobe), while no correlations were observed in the ADAS-cog. With all clinical subgroups combined, voxel-based analysis showed that MMSE performance correlated with [18 F]FDG-UR the temporal and posterior cingulate gyrus cortical metabolism bilaterally, while ADAS-cog performance was correlated with the meso-temporal, temporal, dorsolateral frontal and parietal cortices. MMSE showed correlation with cortical hypometabolism in small cortical regions, in the AD subgroup but not in MCI or EMCI. ADAS-cog was associated with mesotemporal synaptic dysfunction in EMCI and LMCI. In AD, ADAS-cog performance was correlated with [18 F]FDG-UR in inferior parietal, temporal and frontal neocortex. Conclusions: Either ADAS-cog or MMSE scores reflect amyloidosis. When the clinical subgroups were analyzed separately, only ADAS-cog results conveyed synaptic dysfunction in cortical areas expected to be affected by AD. IC-P-084
INTERACTION OF CEREBROVASCULAR LESIONS AND ATROPHY ON BRAIN MRI IN RELATION TO COGNITIVE DECLINE OVER FOUR YEARS IN PEOPLE WITH SYMPTOMATIC ATHEROSCLEROTIC DISEASE: THE SMART-MR STUDY
Minke Kooistra1, Mirjam Geerlings1, Yolanda van der Graaf1, Jaap Kappelle1, Majon Muller2, Geert Jan Biessels1, 1University Medical Center Utrecht, Utrecht, Netherlands; 2National Institute of Health, Amsterdam, Netherlands. Background: Neurodegenerative changes and vascular lesions often co-occur in the brains of older individuals. Together these lesions contribute to cognitive decline and dementia. Several cross-sectional studies, including ours, found an interaction between cerebrovascular pathology and global brain or hippocampal atrophy in relation to cognitive performance in demented and non-demented populations. However, only few studies assessed this interaction longitudinally. Our aim was to investigate the interaction between cerebral atrophy and white matter lesions (WML) in relation to cognitive decline over 4 years of follow-up in patients with symptomatic atherosclerotic disease. Methods: The Second Manifestations of ARTerial disease-Magnetic Resonance (SMART-MR) study is a prospective cohort study among patients with symptomatic atherosclerotic disease (57 6 9 years; 80% men). This study concerns 448 patients from whom a 1.5T MRI and a cognitive assessment was available at baseline and again after a mean (range) follow-up of 3.7 years (2.96 - 4.60). Patients also had an extensive vascular screening. Automated brain segmentation was used to quantify total brain volume, intracranial volume and WML volume. Zscores for cognitive performance were calculated on the domains memory and executive functioning at baseline and follow-up. Results: Linear regression analyses, adjusted for age, sex, education, estimated pre-morbid IQ,
Figure 1. SPM-t-statistics maps representing regression between [18F]FDG UR and ADAS-cog or MMSE overlaid on structural MRI.
follow-up time, brain infarcts and baseline cognitive performance, showed that the association of WML volume with memory decline and decline in executive functioning was modified by cerebral atrophy (p-interaction ¼ 0.008 and 0.054, respectively). In patients with severe brain atrophy (>75%, n ¼ 112), but not in those with little or moderate brain atrophy, higher WML volume was related to a decline in memory (B ¼ -0.12, 95%CI -0.234 to 0.003, p-value ¼ 0.06) and a decline in executive functioning (B ¼ -0.24, 95%CI -0.376 to -0.094, p-value ¼ 0.001). Conclusions: In this large cohort of patients with atherosclerotic disease, greater WML volume is a risk factor for decline in memory and executive functioning after 4 years in the presence of cerebral atrophy. These findings provide further evidence that the effects of neurodegeneration and cerebrovascular pathology interact in the etiology of cognitive decline and dementia.
IC-P-085
SPATIAL HETEROGENEITY OF PATTERNS OF CORTICAL AMYLOID DEPOSITION IN HEALTHY AGING AND ITS RELATIONSHIP TO MEMORY DECLINE
Rachel Yotter1, Jimit Doshi1, Vanessa Clark1, Jitka Sojkova2, Yungui Zhou3, Dean Wong3, Luigi Ferrucci4, Susan Resnick2, Christos Davatzikos1, 1Section for Biomedical Image Analysis, Philadelphia, Pennsylvania, United States; 2Laboratory of Behavioral Neuroscience, Baltimore, Maryland, United States; 3John Hopkins School of Medicine, Baltimore, Maryland, United States; 4Longitudinal Studies Section, Baltimore, Maryland, United States.
Alzheimer’s Imaging Consortium Posters: IC-P
(Table 1). While decreased GMV in the prefrontal and temporal cortices, dorsal anterior cingulate, posterior cingulate and the insula were associated with the main effects of depression, increased GM atrophy in the thalamus, and default mode, executive control and medial temporal lobe (MTL) regions were related to the main effects of aMCI. Depression-aMCI interactive effects were associated with global GM volume loss involving cortical and MTL structures (P<0.05 FDR corrected; Figure 1). Depressive symptoms were negatively correlated and episodic memory performances were positively associated with GMV in similar brain regions as observed with LLD and aMCI respectively. Depressive symptom-memory deficit interactive effects were also seen globally, especially in the DMN and MTL regions. Conclusions: The interactive effects of LLD and aMCI are associated with GMV loss in crucial cognition and mood regulation structures. The co-existence of these clinical phenotypes may be a marker of AD.
IC-P-083
ASSOCIATION BETWEEN BRAIN AMYLOIDOSIS, SYNAPTIC DYSFUNCTION AND COGNITIVE PERFORMANCE MEASURED WITH ADAS-COG AND MMSE SCORES IN EARLY MCI, LATE MCI AND ALZHEIMER’S DISEASE
Marina Dauar1, Jared Rowley2, Liyong Wu3, Monica Shin3, Sara Mohades4, Vladimir Fonov5, Antoine Leuzy6, Serge Gauthier7, Pedro Rosa-Neto8, 1McGill Center for Studies in Aging, Montreal, Quebec, Canada; 2McGill University, Verdun, Quebec, Canada; 3McGill Center for Studies in Aging, Verdun, Quebec, Canada; 4McGill University, Verdun, Quebec, Canada; 5Montreal Neurological Institute, Montreal, Quebec, Canada; 6McGill Centre for Studies in Aging, Montreal, Quebec, Canada; 7 Alzheimer Disease Research Unit, McGill Center for Studies in Aging, Montreal, Quebec, Canada; 8McGill University, Montreal, Quebec, Canada. Background: Mini Mental Status Examination (MMSE) and Alzheimer’s Disease (ADx) Assessment Scale-cognitive subscale (ADAS-cog) are instruments for assessing cognitive deficits in ADx. Although MMSE and ADAS-cog differ in terms of complexity it is possible that both batteries convey comparable information regarding amyloid pathology or neurodegeneration. Here, we aimed to investigate the degree of association between two cognitive scales (ADAS-cog and MMSE), synaptic depletion and fibrillar amyloid deposition measured by [18F]FDG and [18F]AV45 PET, respectively. Methods: We analyzed a subsample of participants from the ADNIGO & ADNI2 who had clinical, neuropsychological, and [18 F] AV45/[18 F]FDG data collected in the course of a single visit. Diagnosis of cognitively normal (CN), early mild cognitive impairment (EMCI), late mild cognitive impairment (LMCI) and Alzheimer’s dementia (AD) was adjusted using ADNI2 guidelines. T1 MRIs underwent non-uniformity correction, were skull-stripped and nonlinearly registered to MNI152 space. After registration to MRI, PET uptake ratios (UR) were calculated by dividing [18 F]AV45 and [18 F]FDG scans by the median counts of cerebellar-gm and pons, respectively. PET images were subsequently registered to MNI152 space. Global [18 F]AV45 and [18 F]FDG estimates were conducted in
Table 1 Demographic information and behavioral performance CN (n ¼ 25) Mean Age (years) Education (years) Gender (F/M) MMSE DRS-2 raw scores Attention INIT/PERS Construct Conceptual Memory Total Paragraph Recall scores IMMED DELAYED HAMA GDS
Dep (n ¼ 18) SD
74.28 15.32
Mean
8.25 2.87
68.61 14.61
28.92
1.22
36.56 36.32 6.00 37.76 23.64 140.36 14.36 12.92 1.16 1.88
SD
aMCI (n ¼ 17)
aMCI/Dep (n ¼ 12)
Mean
Mean
SD
1.83
26.92
13.87 2.99 1.93c
0.043 0.175 0.135 0.001*
75.12 13.47
28.06
1.21
27.29
0.51 1.38 0.00 1.33 1.04 2.53
36.39 36.22 5.94 37.61 23.89 140.11
0.70 2.10 0.24 1.24 1.13 3.20
35.71 34.88 5.94 35.88 19.06 130.88
0.77b 3.62 0.24 2.45b 2.68b,d 5.49b,d
36.00 32.50 5.83 35.41 19.50 129.67
1.21 5.55 0.58 3.12c,e 3.60c,e 6.70c,e,f
0.004* 0.005 0.436 0.001* 0.000* 0.000*
3.73 4.03 1.06 2.11
14.17 12.06 10.88 17.28
3.96 4.24 5.07a 3.29a
8.41 2.47 2.18 4.35
3.59b,d 3.30b,d 1.55d 2.67d
7.17 3.25 8.67 14.25
3.76c,e 3.14c,e 4.19c,f 6.43c,f
0.000* 0.000* 0.000* 0.000*
14/4
68.33 14.25
P
6.81 2.57
12/13
6.62 2.07
SD
11/6
7/5
Notes. Significant differences (p<0.004, Bonferroni correction for multiple comparison) were found in MMSE, DRS-2 raw scores (except for INIT/PERS and Construct), Logical Memory II subscale (Immediate and Delayed Paragraph Recall) from the Wechsler Memory Scale – Revised and emotional scores (HAMA and GDS) among four groups. p values were obtained by one-way ANOVA analysis except for gender (X2 test). a-f: post-hoc analysis (Bonferroni correction) further revealed the source of ANOVA differences (a: CN vs Dep; b: CN vs aMCI; c: CN vs aMCI/Dep; d: Dep vs aMCI; e: Dep vs aMCI/Dep; f: aMCI vs aMCI/ Dep). Unless otherwise indicated, data are presented as mean 6 SD. Abbreviation: CN, cognitive normal; Dep, cognitively normal with late-life depression; aMCI, amnestic mild cognitive impairment; aMCI/Dep, amnestic mild cognitive impairment with late-life depression; M, mean; SD, standard deviation; F/M: female/male; MMSE, mini-mental state examination; DRS-2: dementia rating scale-2; INIT/PERS: Initiation/Preservation; IMMED, immediate recall scores; DELAYED, delayed recall scores; HAMA, Hamilton anxiety scales scores; GDS, geriatric depression scale scores.
Alzheimer’s Imaging Consortium Posters: IC-P
P49
Table 1 Demographic data, global uptake ratio of [18F]AV45 and [18F]FDG for all groups
Gender (M/F) Age (years) Education (years) MMSE CDR ADAS-cog Delayed recall of logical memory Global uptake ratio of AV45 Global uptake ratio of FDG
CN (n ¼ 109)
EMCI (n ¼ 157)
LMCI (n ¼ 39)
AD (n ¼ 49)
P value
53/56 78.8 6 5.9 16.4 6 2.8 29.1 6 1.2 060 6.2 6 4.2 14.0 6 3.7 1.28 6 0.25 1.29 6 0.13
90/67 73.1 6 7.9a 16.0 6 2.7 28.3 6 1.5a 0.5 6 0.1a 7.9 6 3.4a 9.3 6 2.1a 1.40 6 0.33a 1.31 6 0.15
24/15 76.2 6 9.2d 16.4 6 3.2 27.1 6 2.2 a,c 0.5 6 0.1a 12.5 6 5.7 a,c 3.5 6 2.8 a,c 1.56 6 0.36 a,c 1.22 6 0.15b,c
32/18 75.6 6 7.8d 16.7 6 2.8 21.4 6 4.7 a,c,e 1.0 6 0.4 a,c,e 21.8 6 10.3 a,c,e 1.5 6 2.6 a,c,e 1.62 6 0.38 a,c 1.14 6 0.15 a,c,e
0.231 <0.001 0.304 <0.001 <0.001 <0.001 <0.001 <0.001 <0.001
All values are indicated as mean 6 standard deviation except gender. p value indicates the value for the main effect of each group, as assessed with analyses of variance (ANOVA) for each variable except for gender, where a contingency chi-square was performed. Statistics for post hoc 2-by-2 group comparisons are provided as significant differences: a from CN at P<0.01; b from CN at P<0.05; c from EMCI at P<0.01; d from EMCI at P<0.05; e from LMCI at P<0.01. native space grey matter regions. Voxel-based age-corrected regression analysis was calculated from images resampled in MNI152. Results: Demographics are summarized in table 1. For all groups collapsed, [18 F] AV45-UR correlated with MMSE only in CN (temporal lobe), while no correlations were observed in the ADAS-cog. With all clinical subgroups combined, voxel-based analysis showed that MMSE performance correlated with [18 F]FDG-UR the temporal and posterior cingulate gyrus cortical metabolism bilaterally, while ADAS-cog performance was correlated with the meso-temporal, temporal, dorsolateral frontal and parietal cortices. MMSE showed correlation with cortical hypometabolism in small cortical regions, in the AD subgroup but not in MCI or EMCI. ADAS-cog was associated with mesotemporal synaptic dysfunction in EMCI and LMCI. In AD, ADAS-cog performance was correlated with [18 F]FDG-UR in inferior parietal, temporal and frontal neocortex. Conclusions: Either ADAS-cog or MMSE scores reflect amyloidosis. When the clinical subgroups were analyzed separately, only ADAS-cog results conveyed synaptic dysfunction in cortical areas expected to be affected by AD. IC-P-084
INTERACTION OF CEREBROVASCULAR LESIONS AND ATROPHY ON BRAIN MRI IN RELATION TO COGNITIVE DECLINE OVER FOUR YEARS IN PEOPLE WITH SYMPTOMATIC ATHEROSCLEROTIC DISEASE: THE SMART-MR STUDY
Minke Kooistra1, Mirjam Geerlings1, Yolanda van der Graaf1, Jaap Kappelle1, Majon Muller2, Geert Jan Biessels1, 1University Medical Center Utrecht, Utrecht, Netherlands; 2National Institute of Health, Amsterdam, Netherlands. Background: Neurodegenerative changes and vascular lesions often co-occur in the brains of older individuals. Together these lesions contribute to cognitive decline and dementia. Several cross-sectional studies, including ours, found an interaction between cerebrovascular pathology and global brain or hippocampal atrophy in relation to cognitive performance in demented and non-demented populations. However, only few studies assessed this interaction longitudinally. Our aim was to investigate the interaction between cerebral atrophy and white matter lesions (WML) in relation to cognitive decline over 4 years of follow-up in patients with symptomatic atherosclerotic disease. Methods: The Second Manifestations of ARTerial disease-Magnetic Resonance (SMART-MR) study is a prospective cohort study among patients with symptomatic atherosclerotic disease (57 6 9 years; 80% men). This study concerns 448 patients from whom a 1.5T MRI and a cognitive assessment was available at baseline and again after a mean (range) follow-up of 3.7 years (2.96 - 4.60). Patients also had an extensive vascular screening. Automated brain segmentation was used to quantify total brain volume, intracranial volume and WML volume. Zscores for cognitive performance were calculated on the domains memory and executive functioning at baseline and follow-up. Results: Linear regression analyses, adjusted for age, sex, education, estimated pre-morbid IQ,
Figure 1. SPM-t-statistics maps representing regression between [18F]FDG UR and ADAS-cog or MMSE overlaid on structural MRI.
follow-up time, brain infarcts and baseline cognitive performance, showed that the association of WML volume with memory decline and decline in executive functioning was modified by cerebral atrophy (p-interaction ¼ 0.008 and 0.054, respectively). In patients with severe brain atrophy (>75%, n ¼ 112), but not in those with little or moderate brain atrophy, higher WML volume was related to a decline in memory (B ¼ -0.12, 95%CI -0.234 to 0.003, p-value ¼ 0.06) and a decline in executive functioning (B ¼ -0.24, 95%CI -0.376 to -0.094, p-value ¼ 0.001). Conclusions: In this large cohort of patients with atherosclerotic disease, greater WML volume is a risk factor for decline in memory and executive functioning after 4 years in the presence of cerebral atrophy. These findings provide further evidence that the effects of neurodegeneration and cerebrovascular pathology interact in the etiology of cognitive decline and dementia.
IC-P-085
SPATIAL HETEROGENEITY OF PATTERNS OF CORTICAL AMYLOID DEPOSITION IN HEALTHY AGING AND ITS RELATIONSHIP TO MEMORY DECLINE
Rachel Yotter1, Jimit Doshi1, Vanessa Clark1, Jitka Sojkova2, Yungui Zhou3, Dean Wong3, Luigi Ferrucci4, Susan Resnick2, Christos Davatzikos1, 1Section for Biomedical Image Analysis, Philadelphia, Pennsylvania, United States; 2Laboratory of Behavioral Neuroscience, Baltimore, Maryland, United States; 3John Hopkins School of Medicine, Baltimore, Maryland, United States; 4Longitudinal Studies Section, Baltimore, Maryland, United States.