Evidence map›Paper›PMID 20122756›Full record

ArticleNeurobiology of aging2011

Ethanol withdrawal acts as an age-specific stressor to activate cerebellar p38 kinase.

Marianna E Jung, Xiaohua Ju, James W Simpkins, Daniel B Metzger, Liang-Jun Yan, Yi Wen

Open access · greenAbstract readComparative Study
In one paragraph

Article in Neurobiology of aging, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.8field-weighted citation impact, top 34% 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

14 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. JNK Signaling Positively Regulates Acute Ethanol Tolerance inInternational journal of molecular sciences · 2024
    Article
  3. Review
  4. Intermittent hypoxia training blunts cerebrocortical presenilin 1 overexpression and amyloid-β accumulation in ethanol-withdrawn rats.American journal of physiology. Regulatory, integrative and comparative physiology · 2017
    Article
  5. The Role of Presenilin-1 in the Excitotoxicity of Ethanol Withdrawal.The Journal of pharmacology and experimental therapeutics · 2016
    Article
  6. Article
  7. Alcohol Withdrawal and Cerebellar Mitochondria.Cerebellum (London, England) · 2015
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. 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

6 authors at 2 institutions in 1 country.

Marianna E JungDepartment of Pharmacology and Neuroscience, Institute for Aging and Alzheimer's disease, University of North Texas Health Science Center at Fort Worth, 3500 Camp Bowie Blvd., Fort Worth, TX 76107-2699, USA. mjung@hsc.unt.edu
Xiaohua Ju
James W Simpkins
Daniel B Metzger
Liang-Jun Yan
Yi Wen
University of North Texas Health Science Center · USUniversity of North Texas · US

Funding

Effects of Age on Ethanol Withdrawal Toxicity: Mechanisms and TherapyR01AA015982 · NIAAA · UNIVERSITY OF NORTH TEXAS HLTH SCI CTR · PI JUNG, MARIANNA E · 2006 to 2010
$1.4M
Estrogens for Alcoholism &Its Neurological ConsequencesR01AA013864 · NIAAA · UNIVERSITY OF NORTH TEXAS HLTH SCI CTR · PI SIMPKINS, JAMES W. · 2004 to 2008
$1.1M
NIAAA NIH HHS AA013864NIAAA NIH HHS AA015982NIAAA NIH HHS R01 AA013864NIAAA NIH HHS R01 AA015982
6 · The paper itself

Abstract

We investigated whether protein kinase p38 plays a role in the brain-aging changes associated with repeated ethanol withdrawal (EW). Ovariectomized young, middle-age and older rats, with or without 17β-estradiol (E2) implantation, received a 90-day ethanol with repeated withdrawal. They were tested for active pP38 expression in cerebellar Purkinje neurons and whole-cerebellar lysates using immunohistochemistry and enzyme-linked immunosorbent assay, respectively. They were also tested for the Rotarod task to determine the behavioral manifestation of cerebellar neuronal stress and for reactive oxygen species (ROS) and mitochondrial protein carbonyls to determine oxidative mechanisms. Middle-age EW rats showed higher levels of pP38-positive Purkinje neurons/cerebellar lysates, which coincided with increased mitochondrial protein oxidation than other diet/age groups. Exacerbated motor deficit due to age-EW combination also began at the middle-age. In comparison, ROS contents peaked in older EW rats. E2 treatment mitigated each of the EW effects to a different extent. Collectively, pP38 may mediate the brain-aging changes associated with pro-oxidant EW at vulnerable ages and in vulnerable neurons in a manner protected by estrogen.

Indexed as

AgingAnimalsCerebellumEnzyme ActivationEthanolFemaleMaleOxidative Stressp38 Mitogen-Activated Protein KinasesRatsRats, Sprague-DawleySubstance Withdrawal SyndromeEthanolp38 Mitogen-Activated Protein Kinases

Identifiers

PMID20122756
PMCPMC7204394
OpenAlexW1970537875

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.