Amyloid, cerebrovascular disease, and neurodegeneration biomarkers are associated with cognitive trajectories in a racially and ethnically diverse, community-based sample.
Alzheimer's disease
Cerebrovascular disease
Cognitive decline
Neuroimaging
Race/Ethnicity
Journal
Neurobiology of aging
ISSN: 1558-1497
Titre abrégé: Neurobiol Aging
Pays: United States
ID NLM: 8100437
Informations de publication
Date de publication:
09 2022
09 2022
Historique:
received:
19
10
2021
revised:
03
05
2022
accepted:
06
05
2022
pubmed:
10
6
2022
medline:
20
7
2022
entrez:
9
6
2022
Statut:
ppublish
Résumé
We characterized the additive contribution of cerebrovascular biomarkers to amyloid and neurodegeneration biomarkers (AV(N)) when modeling prospective, longitudinal cognitive trajectories within 3 major racial/ethnic groups. Participants (n = 172; age = 69-96 years; 62% women; 31%/49%/20% Non-Hispanic White/Non-Hispanic Black/Hispanic) from the Washington Heights-Inwood Columbia Aging Project were assessed for amyloid (Florbetaben PET), neurodegeneration (cortical thickness, hippocampal volume), and cerebrovascular disease (white matter hyperintensity (WMH), infarcts). Neuropsychological assessments occurred every 2.3 ± 0.6 years for up to 6 visits (follow-up time: 4.2 ± 3.2 years). Linear mixed-effects models were stratified by race/ethnicity groups. Higher amyloid was associated with faster memory decline in all 3 racial/ethnic groups, but was related to faster cognitive decline beyond memory in minoritized racial/ethnic groups. Higher WMH was associated with faster language, processing speed/executive function, and visuospatial ability decline in Non-Hispanic Black participants, while infarcts were associated with faster processing speed/executive function decline in Non-Hispanic White participants. Complementary information from AD, neurodegenerative, and cerebrovascular biomarkers explain decline in multiple cognitive domains, which may differ within each racial/ethnic group. Importantly, treatment strategies exist to minimize vascular contributions to cognitive decline.
Identifiants
pubmed: 35679806
pii: S0197-4580(22)00110-5
doi: 10.1016/j.neurobiolaging.2022.05.004
pmc: PMC9997572
mid: NIHMS1871390
pii:
doi:
Substances chimiques
Amyloid
0
Biomarkers
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
83-96Subventions
Organisme : NIA NIH HHS
ID : R01 AG034189
Pays : United States
Organisme : NIA NIH HHS
ID : R56 AG034189
Pays : United States
Organisme : NIA NIH HHS
ID : R01 AG054520
Pays : United States
Organisme : NIA NIH HHS
ID : P01 AG007232
Pays : United States
Organisme : NIA NIH HHS
ID : RF1 AG054023
Pays : United States
Organisme : NIA NIH HHS
ID : R01 AG037212
Pays : United States
Organisme : NIA NIH HHS
ID : K99 AG065506
Pays : United States
Organisme : NIA NIH HHS
ID : R01 AG072474
Pays : United States
Informations de copyright
Copyright © 2022 Elsevier Inc. All rights reserved.
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