Open AccessAmyloid β influences the relationship between cortical thickness and vascular load
Author(s) -
Parker Thomas D.,
Cash David M.,
Lane Christopher A.,
Lu Kirsty,
Malone Ian B.,
Nicholas Jennifer M.,
James SarahNaomi,
Keshavan Ashvini,
MurraySmith 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.
Publication year - 2020
Publication title -
alzheimer's and dementia: diagnosis, assessment and disease monitoring
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.497
H-Index - 37
ISSN - 2352-8729
DOI - 10.1002/dad2.12022
Subject(s) - positron emission tomography , magnetic resonance imaging , white matter , pathology , pathological , neurodegeneration , neuroimaging , hyperintensity , alzheimer's disease , psychology , neuroscience , medicine , disease , radiology
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 18 F‐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.