Amyloid Hypothesis: Is There a Role for Antiamyloid Treatment in Late-Life Depression?
Open accessAbstract
Antidepressants have modest efficacy in late-life depression (LLD), perhaps because various neurobiologic processes compromise frontolimbic networks required for antidepressant response. We propose that amyloid accumulation is an etiologic factor for frontolimbic compromise that predisposes to depression and increases treatment resistance in a subgroup of older adults. In patients without history of depression, amyloid accumulation during the preclinical phase of Alzheimer disease (AD) may result in the prodromal depression syndrome that precedes cognitive impairment. In patients with early-onset depression, pathophysiologic changes during recurrent episodes may promote amyloid accumulation, further compromise neurocircuitry required for antidepressant response, and increase treatment resistance during successive depressive episodes. The findings that support the amyloid hypothesis of LLD are (1) Depression is a risk factor, a prodrome, and a common behavioral manifestation of AD; (2) amyloid deposition occurs during a long predementia period when depression is prevalent; (3) patients with lifetime history of depression have significant amyloid accumulation in brain regions related to mood regulation; and (4) amyloid deposition leads to neurobiologic processes, including vascular damage, neurodegeneration, neuroinflammation, and disrupted functional connectivity, that impair networks implicated in depression. The amyloid hypothesis of LLD is timely because availability of ligands allows in vivo assessment of amyloid in the human brain, a number of antiamyloid agents are relatively safe, and there is evidence that some antidepressants may reduce amyloid production. A model of LLD introducing the role of amyloid may guide the design of studies aiming to identify novel antidepressant approaches and prevention strategies of AD.
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Amyloid beta accumulation may predispose to late-life depression.
“Several studies suggest that amyloid beta (Aβ) accumulation may predispose to LLD109.”
From Mechanisms and treatment of late-life depression (2019) · cites this paper as [109]
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- Authors
- Mahgoub, N., & Alexopoulos, G. S.
- Affiliations
- Weill Cornell Medicine (US)
- Cornell University (US)
- Corresponding author
- Alexopoulos, George S.
- Venue
- The American Journal of Geriatric Psychiatry
- Publisher
- Elsevier BV
- Published
- 2016-03
- Volume
- 24
- Issue
- 3
- Pages
- 239-247
- ISSN
- 1064-7481 (ISSN-L)
- PMC
- PMC4801691
- OpenAlex
- W2266200372
- Cited by
- 81
- References
- 78
- Citations by year
- 2026: 8 · 2025: 3 · 2024: 9 · 2023: 9 · 2022: 9 · 2021: 11 · 2020: 8 · 2019: 3 · 2018: 10 · 2017: 5 · 2016: 6
- FWCI
- 0.92
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- American Journal of Geriatric Psychiatry (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of Mental Health (P30 MH085943)
- Sanchez Foundation
- Forest
- Topics
- Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Keywords
- amyloid hypothesis, geriatric depression, amyloid accumulation, Alzheimer's disease, antidepressant resistance, prodromal depression, early-onset depression, neuroinflammation, neurodegeneration, vascular injury, functional connectivity, antidepressant response
- MeSH terms
- Late Onset Disorders, Aged, Antidepressive Agents, Brain, Depression, Humans, Models, Neurological, Amyloid beta-Peptides, Prodromal Symptoms
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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