Evidence map›Paper›PMID 23201762›Full record

ReviewNutrients2012

Dysregulation of glutathione homeostasis in neurodegenerative diseases.

William M Johnson, Amy L Wilson-Delfosse, John J Mieyal

Open access · goldAbstract readReview
In one paragraph

Review in Nutrients, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 176 papers.

0numbers the graph read from it
0cells of the map it votes in
176citing papers in PubMed
12.3field-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

176 citing papers in PubMed, 345 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Article
  4. Skin Histology ofAntioxidants (Basel, Switzerland) · 2026
    Article
  5. Review
  6. Review
  7. Metabolic Brain Disorders: Prodromes, Symptoms, and Syndromes.International journal of molecular sciences · 2026
    Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Review
  15. Oxidative Stress onVeterinary sciences · 2025
    Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article

116 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

3 authors at 2 institutions in 1 country.

William M JohnsonDepartment of Pharmacology, Case Western Reserve University, 2109 Adelbert Rd, Cleveland, OH 44106, USA. wmj18@case.edu
Amy L Wilson-Delfosse
John J Mieyal
Louis Stokes Cleveland VA Medical Center · USCase Western Reserve University · US

Funding

PREDOCTORAL TRAINING PROGRAM IN MOLECULAR THERAPEUTICST32GM008803 · NIGMS · CASE WESTERN RESERVE UNIVERSITY · PI MIEYAL, JOHN J, NIEMAN, MARVIN THOMAS · 2001 to 2023
$4.2M
Assay Development and Discovery of LRRK2 Inhibitors for Parkinson DiseaseR21NS073170 · NINDS · CASE WESTERN RESERVE UNIVERSITY · PI CHEN, SHU G. · 2010 to 2011
$428k
Enzymatic Regulation of S-Glutathionylation : Role in Apoptosis and DiseaseI01BX000290 · VA · LOUIS STOKES CLEVELAND VA MEDICAL CENTER · PI MIEYAL, JOHN J · 2011 to 2012
–
BLRD VA I01 BX000290NIGMS NIH HHS T-32 GM008803NIGMS NIH HHS T32 GM008803NINDS NIH HHS NIH R21 5R21NS073170-02NINDS NIH HHS R21 NS073170
6 · The paper itself

Abstract

Dysregulation of glutathione homeostasis and alterations in glutathione-dependent enzyme activities are increasingly implicated in the induction and progression of neurodegenerative diseases, including Alzheimer's, Parkinson's and Huntington's diseases, amyotrophic lateral sclerosis, and Friedreich's ataxia. In this review background is provided on the steady-state synthesis, regulation, and transport of glutathione, with primary focus on the brain. A brief overview is presented on the distinct but vital roles of glutathione in cellular maintenance and survival, and on the functions of key glutathione-dependent enzymes. Major contributors to initiation and progression of neurodegenerative diseases are considered, including oxidative stress, protein misfolding, and protein aggregation. In each case examples of key regulatory mechanisms are identified that are sensitive to changes in glutathione redox status and/or in the activities of glutathione-dependent enzymes. Mechanisms of dysregulation of glutathione and/or glutathione-dependent enzymes are discussed that are implicated in pathogenesis of each neurodegenerative disease. Limitations in information or interpretation are identified, and possible avenues for further research are described with an aim to elucidating novel targets for therapeutic interventions. The pros and cons of administration of N-acetylcysteine or glutathione as therapeutic agents for neurodegenerative diseases, as well as the potential utility of serum glutathione as a biomarker, are critically evaluated.

Indexed as

HomeostasisAcetylcysteineAlzheimer DiseaseAmyotrophic Lateral SclerosisBrainFriedreich AtaxiaGlutathioneHumansHuntington DiseaseNeurodegenerative DiseasesParkinson DiseaseAcetylcysteineGlutathione

Identifiers

PMID23201762
PMCPMC3497002
OpenAlexW1982146336

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.