Evidence map›Paper›PMID 25933648›Full record

ArticleCerebellum (London, England)2015

Effects of Ethanol on the Cerebellum: Advances and Prospects.

Jia Luo

Open access · bronzeAbstract read
In one paragraph

Article in Cerebellum (London, England), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
9.2field-weighted citation impact, top 3% 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

34 citing papers in PubMed, 75 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Reward Neurocircuitry Predicts Longitudinal Changes in Alcohol Use Following Trauma Exposure.Biological psychiatry. Cognitive neuroscience and neuroimaging · 2025
    Article
  5. Article
  6. Alcohol Toxicity in the Developing Cerebellum.Diagnostics (Basel, Switzerland) · 2024
    Article
  7. Article
  8. Article
  9. Machine Learning of Functional Connectivity to Biotype Alcohol and Nicotine Use Disorders.Biological psychiatry. Cognitive neuroscience and neuroimaging · 2024
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Alcohol Withdrawal and the Associated Mood Disorders-A Review.International journal of molecular sciences · 2022
    Review
  17. Article
  18. Article
  19. Review
  20. Mechanisms of Ethanol-Induced Cerebellar Ataxia: Underpinnings of Neuronal Death in the Cerebellum.International journal of environmental research and public health · 2021
    Review
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

1 author at 1 institution in 1 country.

Jia LuoDepartment of Pharmacology and Nutritional Sciences, University of Kentucky College of Medicine, 132 Health Sciences Research Building, 1095 Veterans Drive, Lexington, KY, 40536, USA, jialuo888@uky.edu.
University of Kentucky · US

Funding

GSK3BETA, A MEDIATOR OF ETHANOL NEUROTOXICITYR01AA015407 · NIAAA · WEST VIRGINIA UNIVERSITY · PI JIA LUO · 2005 to 2026
$6.2M
Thiamine deficiency and alcohol-induced neurodegenerationI01BX001721 · VA · VA MEDICAL CENTER - LEXINGTON, KY · PI LUO, JIA · 2014 to 2022
–
BLRD VA I01 BX001721NIAAA NIH HHS AA015407NIAAA NIH HHS R01 AA015407
6 · The paper itself

Abstract

Alcohol abuse causes cerebellar dysfunction and cerebellar ataxia is a common feature in alcoholics. Alcohol exposure during development also impacts the cerebellum. Children with fetal alcohol spectrum disorder (FASD) show many symptoms associated specifically with cerebellar deficits. However, the cellular and molecular mechanisms are unclear. This special issue discusses the most recent advances in the study of mechanisms underlying alcoholinduced cerebellar deficits. The alteration in GABAA receptor-dependent neurotransmission is a potential mechanism for ethanol-induced cerebellar dysfunction. Recent advances indicate ethanol-induced increases in GABA release are not only in Purkinje cells (PCs), but also in molecular layer interneurons and granule cells. Ethanol is shown to disrupt the molecular events at the mossy fiber - granule cell - Golgi cell (MGG) synaptic site and granule cell parallel fibers - PCs (GPP) synaptic site, which may be responsible for ethanol-induced cerebellar ataxia. Aging and ethanol may affect the smooth endoplasmic reticulum (SER) of PC dendrites and cause dendritic regression. Ethanol withdrawal causes mitochondrial damage and aberrant gene modifications in the cerebellum. The interaction between these events may result in neuronal degeneration, thereby contributing to motoric deficit. Ethanol activates doublestranded RNA (dsRNA)-activated protein kinase (PKR) and PKR activation is involved ethanolinduced neuroinflammation and neurotoxicity in the developing cerebellum. Ethanol alters the development of cerebellar circuitry following the loss of PCs, which could result in modifications of the structure and function of other brain regions that receive cerebellar inputs. Lastly, choline, an essential nutrient is evaluated for its potential protection against ethanol-induced cerebellar damages. Choline is shown to ameliorate ethanol-induced cerebellar dysfunction when given before ethanol exposure.

Indexed as

AnimalsCentral Nervous System DepressantsCerebellumDevelopmental DisabilitiesEthanolFemaleHumansNeuronsPregnancyPrenatal Exposure Delayed EffectsCentral Nervous System DepressantsEthanol

Identifiers

PMID25933648
PMCPMC4492805
OpenAlexW2002614030

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.