Evidence mapPaperPMID 40128481Full record

ReviewAdvances in experimental medicine and biology2025

Excessive Alcohol Use as a Risk Factor for Alzheimer's Disease: Epidemiological and Preclinical Evidence.

Paige E Anton, Nicole M Maphis, David N Linsenbardt, Leon G Coleman

Abstract readReview
In one paragraph

Review in Advances in experimental medicine and biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
field-weighted citation impact
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

9 citing papers in PubMed.

  1. Article
  2. 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

4 authors.

Paige E AntonBowles Center for Alcohol Studies, University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, NC, USA.
Nicole M MaphisDepartment of Neurosciences and New Mexico Alcohol Research Center, School of Medicine, University of New Mexico Health Sciences Center, Albuquerque, NM, USA.
David N LinsenbardtDepartment of Neurosciences and New Mexico Alcohol Research Center, School of Medicine, University of New Mexico Health Sciences Center, Albuquerque, NM, USA.
Leon G ColemanBowles Center for Alcohol Studies, University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, NC, USA. leon_coleman@med.unc.edu.

Funding

C7-Pilot Project coreP50AA022534 · NIAAA · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · 2024 to 2025
$4.4M
MOLECULAR AND CELLULAR ALCOHOL RESEARCH TRAININGT32AA007573 · UNIV OF NORTH CAROLINA CHAPEL HILL · 1997 to 2025
$1.6M
Academic Science Education and Research TrainingK12GM088021 · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · 2025 to 2025
$1.2M
Alcohol and Developing Neuronal CircuitsR01AA015614 · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · 2005 to 2025
$784k
Alcohol Research Training: Methods and Mechanisms of ChangeT32AA018108 · UNIVERSITY OF NEW MEXICO · 2025 to 2025
$472k
The Reciprocal Relationship between Binge Drinking and Astrocytic SignalingU54AA030463 · UNIV OF NORTH CAROLINA CHAPEL HILL · 2025 to 2025
$311k
NIAAA NIH HHS K99 AA025120NIAAA NIH HHS P50 AA022534NIAAA NIH HHS R00 AA025120NIAAA NIH HHS R01 AA015614NIAAA NIH HHS R01 AA028924NIAAA NIH HHS R37 AA015614NIAAA NIH HHS T32 AA007573NIAAA NIH HHS T32 AA018108NIAAA NIH HHS U54 AA030463NIGMS NIH HHS K12 GM088021
6 · The paper itself

Abstract

Alcohol use has recently emerged as a modifiable risk factor for Alzheimer's disease (AD). However, the neurobiological mechanisms by which alcohol interacts with AD pathogenesis remain poorly understood. In this chapter, we review the epidemiological and preclinical support for the interaction between alcohol use and AD. We hypothesize that alcohol use increases the rate of accumulation of specific AD-relevant pathologies during the prodromal phase and exacerbates dementia onset and progression. We find that alcohol consumption rates are increasing in adolescence, middle age, and aging populations. In tandem, rates of AD are also on the rise, potentially as a result of this increased alcohol use throughout the lifespan. We then review the biological processes in common between alcohol use disorder and AD as a means to uncover potential mechanisms by which they interact; these include oxidative stress, neuroimmune function, metabolism, pathogenic tauopathy development and spread, and neuronal excitatory/inhibitory balance (EIB). Finally, we provide some forward-thinking suggestions we believe this field should consider. In particular, the inclusion of alcohol use assessments in longitudinal studies of AD and more preclinical studies on alcohol's impacts using better animal models of late-onset Alzheimer's disease (LOAD).

Indexed as

Alcohol DrinkingAlcoholismAlzheimer DiseaseAnimalsHumansOxidative StressRisk FactorsAlzheimer’s diseaseDementiaEthanolExcitationInhibitionMetabolismNeuroimmuneOxidative stress

Identifiers

PMID40128481
PMCPMC12720481

What Socratic holds

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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 Socratic graph.