P3-304: Everyday Cognition Scale Predicts Brain Amyloid Deposition: Preliminary Results From the Argentina-Adni Study

Abstract A blood test that predicts the extent of amyloid plaques in the brain and risk of Alzheimer’s disease would have important benefits for the early identification of higher risk of dementia and Alzheimer’s disease and the evaluation of new preventative therapies. The goal of this study was to determine whether plasma levels of amyloid-β1–42, 1–40 and the amyloid-β1–42/1–40 ratio among participants in the Pittsburgh centre of the Ginkgo Evaluation of Memory Study were related to the extent of brain fibrillar amyloid plaques measured in 2009 using Pittsburgh compound-B PET imaging, hippocampal volume, cortical thickness in the temporal lobe and white matter lesions. There were 194 participants who had Pittsburgh compound-B measurements in 2009 with the mean age of 85 years; 96% were white and 60% men. Pittsburgh compound-B positivity was defined as a standardized uptake value ratio of ≥1.57. Amyloid-β in blood was measured using a sandwich enzyme-linked immunosorbent assay developed by Eli Lilly and modified at the University of Vermont. All participants were nondemented as of 2008 at the time of study close out. The study sample included 160 with blood samples drawn in 2000–02 and 133 from 2009 and also had brain amyloid measured in 2009. All blood samples were analysed at the same time in 2009. Plasma amyloid-β1–42 was inversely related to the percent Pittsburgh compound-B positive (standardized uptake value ratio ≥1.57), β −0.04, P = 0.005. Practically all participants who were apolipoprotein-E4 positive at older ages were also Pittsburgh compound-B positive for fibrillar amyloid. Among apolipoprotein-E4-negative participants, quartiles of amyloid-β1–42 were inversely related to Pittsburgh compound-B positivity. In multiple regression models, plasma amyloid-β1–42 measured in 2000–02 or 2009 were significantly and inversely related to Pittsburgh compound-B positivity as was the amyloid-β1–42/1–40 ratio. There was a 4-fold increase in the odds ratio for the presence of Pittsburgh compound-B positivity in the brain in 2009 for the first quartile of amyloid-β1–42 as compared with the fourth quartile in the multiple logistic model. This is one of the first longitudinal studies to evaluate the relationship between amyloid-β1–42 in the blood and the extent of brain amyloid deposition measured by PET imaging using Pittsburgh compound-B. Our findings showed that remote and recent low plasma amyloid-β1–42 levels were inversely associated with brain amyloid deposition in cognitively normal individuals. However, changes in plasma amyloid-β1–42 over time (8 years) were small and not related to the amount of Pittsburgh compound-B.

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Brain Amyloid Deposition in Late-Life Depression

Biological Psychiatry ◽

10.1016/j.biopsych.2020.07.025 ◽

2020 ◽

Author(s):

Nunzio Pomara ◽

Bruno Pietro Imbimbo

Keyword(s):

Late Life ◽

Amyloid Deposition ◽

Late Life Depression ◽

Brain Amyloid Deposition

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Special lipid-based diets alleviate cognitive deficits in the APPswe/PS1dE9 transgenic mouse model of Alzheimer's disease independent of brain amyloid deposition

The Journal of Nutritional Biochemistry ◽

10.1016/j.jnutbio.2013.09.015 ◽

2014 ◽

Vol 25 (2) ◽

pp. 157-169 ◽

Cited By ~ 29

Author(s):

Hennariikka Koivisto ◽

Marcus O. Grimm ◽

Tatjana L. Rothhaar ◽

Róbert Berkecz ◽

Dieter Lütjohann ◽

...

Keyword(s):

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Mouse Model ◽

Transgenic Mouse ◽

Cognitive Deficits ◽

Transgenic Mouse Model ◽

Amyloid Deposition ◽

Model Of Alzheimer’S Disease ◽

Brain Amyloid Deposition

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P2-342: THE EFFECT OF RACE ON THE ASSOCIATION BETWEEN WHITE MATTER STRUCTURE AND BRAIN AMYLOID DEPOSITION: THE ARIC-PET STUDY

Alzheimer s & Dementia ◽

10.1016/j.jalz.2019.06.2749 ◽

2019 ◽

Vol 15 ◽

pp. P724-P726

Author(s):

Keenan A. Walker ◽

Yun Zhou ◽

Timothy M. Hughes ◽

Clifford R. Jack ◽

David S. Knopman ◽

...

Keyword(s):

White Matter ◽

Amyloid Deposition ◽

Brain Amyloid Deposition

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Abstract P321: Is Amyloid Deposition in the Brain of Non-demented Older Adults a Consequence of High Blood Pressure and Arterial Stiffness?

Circulation ◽

10.1161/circ.127.suppl_12.ap321 ◽

2013 ◽

Vol 127 (suppl_12) ◽

Author(s):

Timothy M Hughes ◽

Lewis H Kuller ◽

Emma J Barinas-Mitchell ◽

Rachel H Mackey ◽

Eric M McDade ◽

...

Keyword(s):

Blood Pressure ◽

Older Adults ◽

Small Vessel Disease ◽

Ankle Brachial Index ◽

Amyloid Deposition ◽

Vascular Stiffness ◽

Standard Deviation Increase ◽

The Brain ◽

Brain Amyloid Deposition

Background: Advances in positron emission tomography imaging using amyloid specific ligands (e.g. PiB-PET) provide in vivo measurement of amyloid deposition in the brain, a hallmark of Alzheimer’s disease (AD) and dementia. Hypertension is believed to promote AD through arterial stiffening and cerebrovascular disease. We hypothesize that vascular measures are associated with amyloid in the brain. Methods: We studied 92 participants aged 83-96 in a follow-up of the Gingko Evaluation of Memory (GEM) Study with measures of: structural MRI of the brain; PiB-PET of brain amyloid deposition; resting blood pressure (BP), ankle brachial index (ABI) and mean arterial pressure (MAP); and vascular stiffness in the central (carotid-femoral ( cf PWV) and heart femoral ( hf PWV), peripheral (femoral-ankle ( fa PWV), and mixed (brachial-ankle ( ba PWV)) vascular beds, using a noninvasive and automated waveform analyzer (Colin Co., Komaki, Japan). Before study entry, all participants underwent ApoE-4 genotyping, detailed neuropsychological battery and adjudication of cognition by committee. Participants with a diagnosis of dementia were excluded from the sub-study. Results: Half (44/92) non-demented older adults in this sub-study were PiB+ for amyloid deposition in the brain. Amyloid deposition was associated with ba PWV, systolic BP and MAP. After adjustment for covariates, one standard deviation increase in ba PWV resulted in a 2-fold increase in the odds of being PiB+. ApoE-4 status was not associated with PWV. Additionally, high white matter disease burden, but not total gray matter volume, was associated with increased cf PWV (p<0.01), hf PWV (p=0.03), SBP (p=0.05) and MAP (p=0.06). Conclusions: The adverse effects of hypertension and vascular stiffness on cerebral small vessel disease is one of the most important hypotheses as to the determinants of amyloid deposition and AD. This is the first report of a possible association between vascular stiffness, BP and in vivo amyloid deposition in non-demented individuals.

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