Late-Life Depression Is Associated With Reduced Cortical Amyloid Burden : Findings From the Alzheimer's Disease Neuroimaging Initiative Depression Project
(2021) In Biological Psychiatry 89(8). p.757-765- Abstract
Background: We evaluated the role of cortical amyloid deposition as a factor contributing to memory dysfunction and increased risk of dementia associated with late-life depression (LLD). Methods: A total of 119 older adult participants with a current diagnosis of major depression (LLD) from the Alzheimer's Disease Neuroimaging Initiative (ADNI) Depression Project study and 119 nondepressed (ND) cognitively unimpaired participants matched on age, sex, and APOE genotype were obtained from the ADNI database. Results: Thirty-three percent of LLD participants met ADNI criteria for mild cognitive impairment. Compared with ND individuals, the LLD group exhibited less global amyloid beta (Aβ) accumulation (p = .05). The proportion of amyloid... (More)
Background: We evaluated the role of cortical amyloid deposition as a factor contributing to memory dysfunction and increased risk of dementia associated with late-life depression (LLD). Methods: A total of 119 older adult participants with a current diagnosis of major depression (LLD) from the Alzheimer's Disease Neuroimaging Initiative (ADNI) Depression Project study and 119 nondepressed (ND) cognitively unimpaired participants matched on age, sex, and APOE genotype were obtained from the ADNI database. Results: Thirty-three percent of LLD participants met ADNI criteria for mild cognitive impairment. Compared with ND individuals, the LLD group exhibited less global amyloid beta (Aβ) accumulation (p = .05). The proportion of amyloid positivity in the LLD group was 19.3% compared with 31.1% for the ND participants (p = .02). Among LLD participants, global Aβ was not associated with lifetime number of depressive episodes, lifetime length of depression, length of lifetime selective serotonin reuptake inhibitor use, or lifetime length of untreated depression (p >. 21 for all). Global Aβ was associated with worse memory performance (p = .05). Similar results were found in secondary analyses restricting comparisons to the cognitively unimpaired LLD participants as well as when comparing the LLD group with an ND group that included participants with mild cognitive impairment. Conclusions: Contrary to expectation, the LLD group showed less Aβ deposition than the ND group and Aβ deposition was not associated with depression history characteristics. Aβ was associated with memory, but this relationship did not differ between LLD and ND. Our results suggest that memory deficits and accelerated cognitive decline reported in previous studies of LLD are not due to greater cortical Aβ accumulation.
(Less)
- author
- author collaboration
- organization
- publishing date
- 2021-04
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- Alzheimer's disease, Amyloid, Cognition, Depressive symptoms, Late-life depression, Mild cognitive impairment
- in
- Biological Psychiatry
- volume
- 89
- issue
- 8
- pages
- 9 pages
- publisher
- Elsevier
- external identifiers
-
- pmid:32980132
- scopus:85100173873
- ISSN
- 0006-3223
- DOI
- 10.1016/j.biopsych.2020.06.017
- language
- English
- LU publication?
- yes
- id
- eddd3719-9215-4740-8be1-98aa1acb853c
- date added to LUP
- 2021-12-22 10:31:25
- date last changed
- 2024-05-19 20:17:14
@article{eddd3719-9215-4740-8be1-98aa1acb853c,
abstract = {{<p>Background: We evaluated the role of cortical amyloid deposition as a factor contributing to memory dysfunction and increased risk of dementia associated with late-life depression (LLD). Methods: A total of 119 older adult participants with a current diagnosis of major depression (LLD) from the Alzheimer's Disease Neuroimaging Initiative (ADNI) Depression Project study and 119 nondepressed (ND) cognitively unimpaired participants matched on age, sex, and APOE genotype were obtained from the ADNI database. Results: Thirty-three percent of LLD participants met ADNI criteria for mild cognitive impairment. Compared with ND individuals, the LLD group exhibited less global amyloid beta (Aβ) accumulation (p = .05). The proportion of amyloid positivity in the LLD group was 19.3% compared with 31.1% for the ND participants (p = .02). Among LLD participants, global Aβ was not associated with lifetime number of depressive episodes, lifetime length of depression, length of lifetime selective serotonin reuptake inhibitor use, or lifetime length of untreated depression (p >. 21 for all). Global Aβ was associated with worse memory performance (p = .05). Similar results were found in secondary analyses restricting comparisons to the cognitively unimpaired LLD participants as well as when comparing the LLD group with an ND group that included participants with mild cognitive impairment. Conclusions: Contrary to expectation, the LLD group showed less Aβ deposition than the ND group and Aβ deposition was not associated with depression history characteristics. Aβ was associated with memory, but this relationship did not differ between LLD and ND. Our results suggest that memory deficits and accelerated cognitive decline reported in previous studies of LLD are not due to greater cortical Aβ accumulation.</p>}},
author = {{Mackin, R. Scott and Insel, Philip S. and Landau, Susan and Bickford, David and Morin, Ruth and Rhodes, Emma and Tosun, Duygu and Rosen, Howie J. and Butters, Meryl and Aisen, Paul and Raman, Rema and Saykin, Andrew and Toga, Arthur and Jack, Clifford and Koeppe, Robert and Weiner, Michael W. and Nelson, Craig}},
issn = {{0006-3223}},
keywords = {{Alzheimer's disease; Amyloid; Cognition; Depressive symptoms; Late-life depression; Mild cognitive impairment}},
language = {{eng}},
number = {{8}},
pages = {{757--765}},
publisher = {{Elsevier}},
series = {{Biological Psychiatry}},
title = {{Late-Life Depression Is Associated With Reduced Cortical Amyloid Burden : Findings From the Alzheimer's Disease Neuroimaging Initiative Depression Project}},
url = {{http://dx.doi.org/10.1016/j.biopsych.2020.06.017}},
doi = {{10.1016/j.biopsych.2020.06.017}},
volume = {{89}},
year = {{2021}},
}