Association between depression, gender and Alzheimer's neuropathology in older adults without dementia.

Alzheimer's disease amyloid late life depression neuropathology sex differences tau

Journal

International journal of geriatric psychiatry
ISSN: 1099-1166
Titre abrégé: Int J Geriatr Psychiatry
Pays: England
ID NLM: 8710629

Informations de publication

Date de publication:
25 Aug 2022
Historique:
received: 15 12 2021
accepted: 22 08 2022
entrez: 1 9 2022
pubmed: 2 9 2022
medline: 2 9 2022
Statut: aheadofprint

Résumé

Previous studies regarding the relationship between depression and Alzheimer's neuropathology in older adults without dementia have reported conflicting findings. This study examined whether depression is associated with Alzheimer's neuropathology and whether sex moderates these relationships. This is a cross-sectional study of older adults without dementia (normal cognition or mild cognitive impairment, age 50+; CDR ≤ 0.5) who had autopsy within 1 year of their last clinic visit in the National Alzheimer's Coordinating Center database (2005-2020). Logistic regression models were fitted to determine if a recent or remote history of depression was associated with amyloid spread beyond the neocortex measured by modified Thal phase score, density of amyloid plaques measured by CERAD score or tau neuropathology measured by modified Braak score. A moderator analysis was performed to determine if any of these associations were moderated by sex. This study included 407 participants (96 Thal, 405 Braak, and 406 CERAD). Those who had recently active depression (within previous 2 years) but not remote depression only were more likely to have higher Thal phase score compared to those without a history of depression (OR = 3.74; 95% CI, 1.15-12.17; p = 0.028). Sex did not moderate this association. No significant associations between recent depression and Braak or CERAD scores were observed. Our findings indicate that the association between late life depression and Alzheimer's neuropathology is associated with spread of amyloid pathology beyond the neocortex to include allocortical and subcortical regions critical for regulation of mood and motivated behavior.

Identifiants

pubmed: 36047339
doi: 10.1002/gps.5809
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : NIA NIH HHS
ID : U01 AG016976
Pays : United States
Organisme : NIA NIH HHS
ID : U24 AG072122
Pays : United States
Organisme : CIHR
ID : FRN PJT - 166134
Pays : Canada

Informations de copyright

© 2022 John Wiley & Sons Ltd.

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Auteurs

Doyoung Kim (D)

Neuropsychopharmacology Research Group, Sunnybrook Research Institute, Toronto, Ontario, Canada.
Department of Pharmacology and Toxicology, University of Toronto, Toronto, Ontario, Canada.

Alex Kiss (A)

ICES, Toronto, Ontario, Canada.
Institute of Health Policy, Management, and Evaluation, Dalla Lana School of Public Health, University of Toronto, Toronto, Ontario, Canada.

Susan E Bronskill (SE)

ICES, Toronto, Ontario, Canada.
Institute of Health Policy, Management, and Evaluation, Dalla Lana School of Public Health, University of Toronto, Toronto, Ontario, Canada.

Krista L Lanctôt (KL)

Neuropsychopharmacology Research Group, Sunnybrook Research Institute, Toronto, Ontario, Canada.
Department of Pharmacology and Toxicology, University of Toronto, Toronto, Ontario, Canada.
Department of Psychiatry, University of Toronto, Toronto, Ontario, Canada.

Nathan Herrmann (N)

Neuropsychopharmacology Research Group, Sunnybrook Research Institute, Toronto, Ontario, Canada.
Department of Psychiatry, University of Toronto, Toronto, Ontario, Canada.

Damien Gallagher (D)

Neuropsychopharmacology Research Group, Sunnybrook Research Institute, Toronto, Ontario, Canada.
Department of Psychiatry, University of Toronto, Toronto, Ontario, Canada.

Classifications MeSH