Evidence map›Paper›PMID 25175868›Full record

ReviewInternational review of neurobiology2014

Neuroimmune basis of alcoholic brain damage.

Fulton T Crews, Ryan P Vetreno

Abstract readReview
In one paragraph

Review in International review of neurobiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 109 papers.

0numbers the graph read from it
0cells of the map it votes in
109citing papers in PubMed
37.3field-weighted citation impact, top 1% 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

109 citing papers in PubMed, 160 citations in OpenAlex.

  1. Trial
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  11. Astrocyte Reactivity by Alcohol Dependence in the Central Amygdala.bioRxiv : the preprint server for biology · 2026
    Article
  12. Review
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49 more citing papers are in PubMed but not listed here.

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.

Fulton T CrewsBowles Center for Alcohol Studies, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA. Electronic address: ftcrews@med.unc.edu.
Ryan P VetrenoBowles Center for Alcohol Studies, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.
University of North Carolina at Chapel Hill · US

Funding

UNC ARC Information/Dissemination CoreP60AA011605 · NIAAA · UNIV OF NORTH CAROLINA CHAPEL HILL · PI Melissa A Herman · 2003 to 2026
$46.3M
Supplement to Molecular and Cellular Studies on Alcohol's ActionsT32AA007573 · NIAAA · UNIV OF NORTH CAROLINA CHAPEL HILL · PI FULTON T CREWS, Thomas L. Kash · 1997 to 2026
$9.3M
UNC-CH NADIA Underage Drinking and Adult Brain Morphology in RatsU01AA020023 · NIAAA · UNIV OF NORTH CAROLINA CHAPEL HILL · PI CREWS, FULTON T · 2010 to 2024
$7.5M
UNC-CH NADIA Administrative CoreU24AA020024 · NIAAA · UNIV OF NORTH CAROLINA CHAPEL HILL · PI CREWS, FULTON T · 2010 to 2024
$6.6M
MOLECULAR AND CELLULAR PATHOGENESIS IN ALCOHOLISMP50AA011605 · NIAAA · UNIVERSITY OF NORTH CAROLINA CHAPEL HILL · PI CREWS, FULTON T · 1998 to 2002
$4.9M
UNC-CH NADIA Scientific CoreU24AA020022 · NIAAA · UNIV OF NORTH CAROLINA CHAPEL HILL · PI CREWS, FULTON T · 2010 to 2014
$2.2M
Pregnane X receptor (PRX)-dependent mechanisms of alcoholic liver diseaseU54AA019767 · NIAAA · UNIV OF NORTH CAROLINA CHAPEL HILL · PI CREWS, FULTON T · 2010 to 2019
$2.1M
Adult neurobiology following adolescent drinkingF32AA021040 · NIAAA · UNIV OF NORTH CAROLINA CHAPEL HILL · PI VETRENO, RYAN PETER · 2012 to 2013
$101k
NIAAA NIH HHS F32 AA021040NIAAA NIH HHS P50 AA011605NIAAA NIH HHS P60 AA011605NIAAA NIH HHS T32 AA007573NIAAA NIH HHS U01 AA020023NIAAA NIH HHS U24 AA020022NIAAA NIH HHS U24 AA020024NIAAA NIH HHS U54 AA019767
6 · The paper itself

Abstract

Alcohol-induced brain damage likely contributes to the dysfunctional poor decisions associated with alcohol dependence. Human alcoholics have a global loss of brain volume that is most severe in the frontal cortex. Neuroimmune gene induction by binge drinking increases neurodegeneration through increased oxidative stress, particularly NADPH oxidase-induced oxidative stress. In addition, HMGB1-TLR4 and innate immune NF-κB target genes are increased leading to persistent and sensitized neuroimmune responses to ethanol and other agents that release HMGB1 or directly stimulate TLR receptors and/or NMDA receptors. Neuroimmune signaling and glutamate excitotoxicity are linked to alcoholic neurodegeneration. Models of adolescent alcohol abuse lead to significant frontal cortical degeneration and show the most severe loss of hippocampal neurogenesis. Adolescence is a period of high risk for ethanol-induced neurodegeneration and alterations in brain structure, gene expression, and maturation of adult phenotypes. Together, these findings support the hypothesis that adolescence is a period of risk for persistent and long-lasting increases in brain neuroimmune gene expression that promote persistent and long-term increases in alcohol consumption, neuroimmune gene induction, and neurodegeneration that we find associated with alcohol use disorders.

Indexed as

Brain InjuriesAlcoholsAnimalsGene Expression RegulationHumansMonocytesNeuroimmunomodulationSignal TransductionAlcoholsCytokinesEthanolHMGB1MicrogliaToll-like receptors

Identifiers

PMID25175868
PMCPMC5765863
OpenAlexW2395422150

What OpenQuestion holds

Textmetadata
LicenceTDM
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.