Affiliations: [a] Albert Einstein College of Medicine, Bronx, NY, USA
| [b] Department of Neurology, Albert Einstein College of Medicine and Montefiore Medical Center, Bronx, NY, USA
| [c] Saul R. Korey, Department of Neurology, Albert Einstein College of Medicine and Montefiore Medical Center, Bronx, NY, USA
Correspondence:
[*]
Correspondence to: Mariel Rubin-Norowitz, Albert Einstein College of Medicine, 1225 Morris Park Avenue, Van Etten 3C, Bronx, NY 10461, USA. Tel.: +1 718 430 3885; Fax: +1 718 430 3870; E-mail: [email protected].
Note: [1] Data used in preparation of this article were obtained from the Alzheimer’s Disease Neuroimaging Initiative (ADNI) database (https://adni.loni.usc.edu). As such, the investigators within the ADNI contributed to the design and implementation of ADNI and/or provided data but did not participate in analysis or writing of this report. A complete listing of ADNI investigators can be found at
https://adni.loni.usc.edu/wp-content/uploads/how_to_apply/ADNI_Acknowledgement_List.pdf
Abstract: Background:Depression is a late-life risk factor for cognitive decline. Evidence suggests an association between Alzheimer’s disease (AD) associated pathologic changes and depressive symptoms. Objective:To investigate the influence of AT(N) biomarker profile (amyloid-β [A], p-tau [T], and neurodegeneration [N]) and gender on cross-sectional associations between subclinical depressive symptoms and cognitive function among older adults without dementia. Methods:Participants included 868 individuals without dementia from the Alzheimer’s Disease Neuroimaging Initiative (ADNI). Depressive symptoms were measured using the Geriatric Depression Scale (GDS). ADNI neuropsychological composite scores assessed memory and executive function (EF). PET, cerebrospinal fluid, and MRI modalities classified the study sample into biomarker profiles: normal biomarkers (A–T–N–), AD continuum (A+T±N±), and suspect non-AD pathology (SNAP; A–T±N–or A–T–N±). Multivariate regression models were used to investigate associations between GDS and cognitive domains. Results:GDS was negatively associated with memory (β= –0.156, p < 0.001) and EF (β= –0.147, p < 0.001) in the whole sample. When classified by biomarker profile, GDS was negatively associated with memory and EF in AD continuum (memory: β= –0.174, p < 0.001; EF: β= –0.129 p = 0.003) and SNAP (memory: β= –0.172, p = 0.005; EF: β= –0.197, p = 0.001) subgroups. When stratified by sex, GDS was negatively associated with memory (β= –0.227, p < 0.001) and EF (β= –0.205, p < 0.001) in men only. Conclusion:The association between subclinical depressive symptoms and cognitive function is highly influenced by the AT(N) biomarker profile.
Keywords: Alzheimer’s disease, amyloid, biomarker, cognition, depressive symptoms, neurodegeneration, tau
