Amyloid β influences the relationship between cortical thickness and vascular load

Introduction Cortical thickness has been proposed as a biomarker of Alzheimer's disease (AD)– related neurodegeneration, but the nature of its relationship with amyloid beta (Aβ) deposition and white matter hyperintensity volume (WMHV) in cognitively normal adults is unclear. Methods We investi...

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Published in:Alzheimer's & dementia : diagnosis, assessment & disease monitoring assessment & disease monitoring, 2020, Vol.12 (1), p.e12022-n/a
Main Authors: Parker, Thomas D., Cash, David M., Lane, Christopher A., Lu, Kirsty, Malone, Ian B., Nicholas, Jennifer M., James, Sarah‐Naomi, Keshavan, Ashvini, Murray‐Smith, Heidi, Wong, Andrew, Buchanan, Sarah M., Keuss, Sarah E., Sudre, Carole H., Thomas, David L., Crutch, Sebastian J., Fox, Nick C., Richards, Marcus, Schott, Jonathan M.
Format: Article
Language:English
Subjects:
Alzheimer's disease
amyloid
Automation
biomarker
Biomarkers
Cognitive ability
cognitively normal
cortical thickness
Dementia
Educational attainment
Magnetic resonance imaging
Memory
MRC National Survey of Health and Development
Neurodegeneration
Neuroimaging
Quality control
Questionnaires
Standard deviation
Tomography
white matter hyperintensities
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Summary:Introduction Cortical thickness has been proposed as a biomarker of Alzheimer's disease (AD)– related neurodegeneration, but the nature of its relationship with amyloid beta (Aβ) deposition and white matter hyperintensity volume (WMHV) in cognitively normal adults is unclear. Methods We investigated the influences of Aβ status (negative/positive) and WMHV on cortical thickness in 408 cognitively normal adults aged 69.2 to 71.9 years who underwent 18F‐Florbetapir positron emission tomography (PET) and structural magnetic resonance imaging (MRI). Two previously defined Alzheimer's disease (AD) cortical signature regions and the major cortical lobes were selected as regions of interest (ROIs) for cortical thickness. Results Higher WMHV, but not Aβ status, predicted lower cortical thickness across all participants, in all ROIs. Conversely, when Aβ‐positive participants were considered alone, higher WMHV predicted higher cortical thickness in a temporal AD‐signature region. Discussion WMHV may differentially influence cortical thickness depending on the presence or absence of Aβ, potentially reflecting different pathological mechanisms.
ISSN:2352-8729
2352-8729
DOI:10.1002/dad2.12022