Evidence map›Paper›PMID 25188266›Full record

ArticlePloS one2014

Differential sensitivity of prefrontal cortex and hippocampus to alcohol-induced toxicity.

Anna-Kate Fowler, Jeremy Thompson, Lixia Chen, Marisela Dagda, Janet Dertien, Katina Sylvestre S Dossou, Ruin Moaddel, Susan E Bergeson, Inna I Kruman

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
1.5field-weighted citation impact, top 21% 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

31 citing papers in PubMed, 60 citations in OpenAlex.

  1. Quantification of the neuropathology of alcohol use disorder using tissue microarrays.Journal of neuropathology and experimental neurology · 2026
    Article
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  3. Forensic neuropathology: 2026 update.Free neuropathology · 2026
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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

9 authors at 3 institutions in 1 country.

Anna-Kate FowlerDepartment of Pharmacology and Neuroscience, Texas Tech University Health Sciences Center, Lubbock, Texas, United States of America.
Jeremy ThompsonDepartment of Pharmacology and Neuroscience, Texas Tech University Health Sciences Center, Lubbock, Texas, United States of America.
Lixia ChenDepartment of Pharmacology and Neuroscience, Texas Tech University Health Sciences Center, Lubbock, Texas, United States of America.
Marisela DagdaDepartment of Pharmacology and Neuroscience, Texas Tech University Health Sciences Center, Lubbock, Texas, United States of America.
Janet DertienDepartment of Pharmacology and Neuroscience, Texas Tech University Health Sciences Center, Lubbock, Texas, United States of America.
Katina Sylvestre S DossouLaboratory of Clinical Investigation, NIA, National Institutes of Health, Baltimore, Maryland, United States of America.
Ruin MoaddelLaboratory of Clinical Investigation, NIA, National Institutes of Health, Baltimore, Maryland, United States of America.
Susan E BergesonDepartment of Pharmacology and Neuroscience, Texas Tech University Health Sciences Center, Lubbock, Texas, United States of America.
Inna I KrumanDepartment of Pharmacology and Neuroscience, Texas Tech University Health Sciences Center, Lubbock, Texas, United States of America.
Texas Tech University Health Sciences Center · USTexas Tech University · USNational Institutes of Health · US

Funding

Intramural NIH HHS
6 · The paper itself

Abstract

The prefrontal cortex (PFC) is a brain region responsible for executive functions including working memory, impulse control and decision making. The loss of these functions may ultimately lead to addiction. Using histological analysis combined with stereological technique, we demonstrated that the PFC is more vulnerable to chronic alcohol-induced oxidative stress and neuronal cell death than the hippocampus. This increased vulnerability is evidenced by elevated oxidative stress-induced DNA damage and enhanced expression of apoptotic markers in PFC neurons. We also found that one-carbon metabolism (OCM) impairment plays a significant role in alcohol toxicity to the PFC seen from the difference in the effects of acute and chronic alcohol exposure on DNA repair and from exaggeration of the damaging effects upon additional OCM impairment in mice deficient in a key OCM enzyme, methylenetetrahydrofolate reductase (MTHFR). Given that damage to the PFC leads to loss of executive function and addiction, our study may shed light on the mechanism of alcohol addiction.

Indexed as

Acute DiseaseAlcoholismAnimalsApoptosisBiomarkersChronic DiseaseDNA DamageDNA RepairEthanolGene ExpressionHippocampusHomocysteineMaleMethylenetetrahydrofolate Reductase (NADPH2)MiceMice, Inbred C57BLBiomarkersEthanolHomocysteineMethylenetetrahydrofolate Reductase (NADPH2)Microtubule-Associated ProteinsMtap2 protein, mouse

Identifiers

PMID25188266
PMCPMC4154772
OpenAlexW2075748018

What OpenQuestion holds

Textmetadata
LicenceCC0
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.