Evidence map›Paper›PMID 26946981›Full record

ReviewThe American journal of geriatric psychiatry : official journal of the American Association for Geriatric Psychiatry2016

Amyloid Hypothesis: Is There a Role for Antiamyloid Treatment in Late-Life Depression?

Nahla Mahgoub, George S Alexopoulos

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in The American journal of geriatric psychiatry : official journal of the American Association for Geriatric Psychiatry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 4 pooled it
4.7field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

42 citing papers in PubMed, 4 syntheses or guidelines pooled it, 78 citations in OpenAlex.

  1. Pooled it
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  7. Preliminary Evidence That Cortical Amyloid Burden Predicts Poor Response to Antidepressant Medication Treatment in Cognitively Intact Individuals With Late-Life Depression.The American journal of geriatric psychiatry : official journal of the American Association for Geriatric Psychiatry · 2021
    Trial
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  10. Remission is insufficient: predictors and mechanistic models of recurrence in late-life depression.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
    Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Nahla MahgoubDepartment of Psychiatry, Weill Cornell Medical College, White Plains, NY.
George S AlexopoulosDepartment of Psychiatry, Weill Cornell Medical College, White Plains, NY. Electronic address: gsalexop@med.cornell.edu.
Cornell University · US

Funding

Research Methods CoreP30MH085943 · NIMH · WEILL MEDICAL COLL OF CORNELL UNIV · PI ALEXOPOULOS, GEORGE S · 2009 to 2013
$9.2M
NIMH NIH HHS P30 MH085943
6 · The paper itself

Abstract

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.

Indexed as

Models, NeurologicalAgedAmyloid beta-PeptidesAntidepressive AgentsBrainDepressionHumansLate Onset DisordersProdromal SymptomsAmyloid beta-PeptidesAntidepressive AgentsAlzheimer diseaseAmyloid hypothesisAntiamyloid agentsLate-life depression

Identifiers

PMID26946981
PMCPMC4801691
OpenAlexW2266200372

What OpenQuestion holds

Textmetadata
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Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.