Evidence map›Paper›PMID 21484198›Full record

ArticleJournal of neurodevelopmental disorders2011

Glutathione pathway gene variation and risk of autism spectrum disorders.

Katherine Bowers, Qing Li, Joseph Bressler, Dimitrios Avramopoulos, Craig Newschaffer, M Daniele Fallin

Open access · hybridAbstract read
In one paragraph

Article in Journal of neurodevelopmental disorders, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.7field-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

36 citing papers in PubMed, 60 citations in OpenAlex.

  1. Trial
  2. Mercury-induced excitotoxicity in autism spectrum disorder: disruption of glutamatergic homeostasis and the therapeutic role of the selenium-glutathione axis.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026
    Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. DNA methylation at birth and lateral ventricular volume in childhood: a neuroimaging epigenetics study.Journal of child psychology and psychiatry, and allied disciplines · 2024
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Oxidative Stress in Autism Spectrum Disorder.Molecular neurobiology · 2020
    Review
  19. Article
  20. 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

6 authors at 4 institutions in 1 country.

Katherine BowersDepartment of Epidemiology, Johns Hopkins Bloomberg School of Public Health, 615 N. Wolfe St. room W6509, Baltimore, MD, 21205, USA.
Qing Li
Joseph Bressler
Dimitrios Avramopoulos
Craig Newschaffer
M Daniele Fallin
Johns Hopkins University · USDrexel University · USJohns Hopkins Medicine · USKennedy Krieger Institute · US

Funding

Center for Genomic and Phenomic Studies in AutismU24MH081810 · NIMH · UNIVERSITY OF SOUTHERN CALIFORNIA · PI LAJONCHERE, CLARA M · 2007 to 2011
$8.3M
NIMH NIH HHS U24 MH081810
6 · The paper itself

Abstract

Despite evidence that autism is highly heritable with estimates of 15 or more genes involved, few studies have directly examined associations of multiple gene interactions. Since inability to effectively combat oxidative stress has been suggested as a mechanism of autism, we examined genetic variation 42 genes (308 single-nucleotide polymorphisms (SNPs)) related to glutathione, the most important antioxidant in the brain, for both marginal association and multi-gene interaction among 318 case-parent trios from The Autism Genetic Resource Exchange. Models of multi-SNP interactions were estimated using the trio Logic Regression method. A three-SNP joint effect was observed for genotype combinations of SNPs in glutaredoxin, glutaredoxin 3 (GLRX3), and cystathione gamma lyase (CTH); OR = 3.78, 95% CI: 2.36, 6.04. Marginal associations were observed for four genes including two involved in the three-way interaction: CTH, alcohol dehydrogenase 5, gamma-glutamylcysteine synthetase, catalytic subunit and GLRX3. These results suggest that variation in genes involved in counterbalancing oxidative stress may contribute to autism, though replication is necessary.

Identifiers

PMID21484198
PMCPMC3188290
OpenAlexW2037593344

What OpenQuestion holds

Textmetadata
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.