Evidence map›Paper›PMID 19507062›Full record

ReviewMolecular neurobiology2009

GSK3beta in ethanol neurotoxicity.

Jia Luo

Abstract readReview
In one paragraph

Review in Molecular neurobiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

52 citing papers in PubMed, 75 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Review
  14. Review
  15. Article
  16. Function and Mechanism of Myelin Regulation in Alcohol Abuse and Alcoholism.BioEssays : news and reviews in molecular, cellular and developmental biology · 2019
    Review
  17. Review
  18. Article
  19. GSK3β in the prefrontal cortex: a molecular handle specific to addiction pathology?Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2018
    Article
  20. Article
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 Internal Medicine, University of Kentucky College of Medicine, 124C Combs Research Building, 800 Rose Street, 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
ALCOHOL AND BREAST CANCERR01AA017226 · NIAAA · WEST VIRGINIA UNIVERSITY · PI LUO, JIA · 2008 to 2024
$5.2M
NIAAA NIH HHS AA015407NIAAA NIH HHS AA017226NIAAA NIH HHS R01 AA015407NIAAA NIH HHS R01 AA017226
6 · The paper itself

Abstract

Alcohol consumption during pregnancy is a significant public health problem and may result in a wide range of adverse outcomes for the child. The developing central nervous system (CNS) is particularly susceptible to ethanol toxicity. Children with fetal alcohol spectrum disorders (FASD) have a variety of cognitive, behavioral, and neurological impairments. FASD currently represents the leading cause of mental retardation in North America ahead of Down syndrome and cerebral palsy. Ethanol exposure during development causes multiple abnormalities in the brain such as permanent loss of neurons, ectopic neurons, and alterations in synaptogenesis and myelinogenesis. These alcohol-induced structural alterations in the developing brain underlie many of the behavioral deficits observed in FASD. The cellular and molecular mechanisms of ethanol neurotoxicity, however, remain unclear. Ethanol elicits cellular stresses, including oxidative stress and endoplasmic reticulum stress. Glycogen synthase kinase 3beta (GSK3beta), a multifunctional serine/threonine kinase, responds to various cellular stresses. GSK3beta is particularly abundant in the developing CNS, and regulates diverse developmental events in the immature brain, such as neurogenesis and neuronal differentiation, migration, and survival. Available evidence indicates that the activity of GSK3beta in the CNS is affected by ethanol. GSK3beta inhibition provides protection against ethanol neurotoxicity, whereas high GSK3beta activity/expression sensitizes neuronal cells to ethanol-induced damages. It appears that GSK3beta is a converging signaling point that mediates some of ethanol's neurotoxic effects.

Indexed as

AnimalsCentral Nervous System DepressantsEthanolFemaleFetal Alcohol Spectrum DisordersGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHumansNerve DegenerationPregnancyPrenatal Exposure Delayed EffectsCentral Nervous System DepressantsEthanolGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGSK3B protein, human

Identifiers

PMID19507062
PMCPMC4993023
OpenAlexW2069179155

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.