ArticleBMC genetics2006
Analysis of case-parent trios at a locus with a deletion allele: association of GSTM1 with autism.
Article in BMC genetics, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled 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.
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.
Who cites it
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 74 citations in OpenAlex.
- Environmental toxicants and autism spectrum disorders: a systematic review.Translational psychiatry · 2014Pooled it
- An Open-Label Case Series of Glutathione Use for Symptomatic Management in Children with Autism Spectrum Disorder.Medical sciences (Basel, Switzerland) · 2023Trial
- Review
- Interactive associations of eczema with glutathione S-transferase genes in relation to autism spectrum disorder and its severity in Jamaican children.Research in autism spectrum disorders · 2023Article
- Article
- Glutathione S-Transferase Polymorphisms and Clinical Characteristics in Autism Spectrum Disorders.Frontiers in psychiatry · 2021Article
- Interaction of glutathione S-transferase polymorphisms and tobacco smoking during pregnancy in susceptibility to autism spectrum disorders.Scientific reports · 2019Article
- Metabolome signature of autism in the human prefrontal cortex.Communications biology · 2019Article
- The role of oxidative stress, inflammation and acetaminophen exposure from birth to early childhood in the induction of autism.The Journal of international medical research · 2017Review
- Modulation of the genome and epigenome of individuals susceptible to autism by environmental risk factors.International journal of molecular sciences · 2015Review
- Interaction betweenResearch in autism spectrum disorders · 2015Article
- Transcriptomic changes in the frontal cortex associated with paternal age.Molecular autism · 2014Article
- Pre-clinical models of neurodevelopmental disorders: focus on the cerebellum.Reviews in the neurosciences · 2014Review
- Autism and phthalate metabolite glucuronidation.Journal of autism and developmental disorders · 2013Article
- Newborn screening for autism: in search of candidate biomarkers.Biomarkers in medicine · 2013Article
- The potential role of the antioxidant and detoxification properties of glutathione in autism spectrum disorders: a systematic review and meta-analysis.Nutrition & metabolism · 2012Article
- Novel metabolic biomarkers related to sulfur-dependent detoxification pathways in autistic patients of Saudi Arabia.BMC neurology · 2011Article
- Glutathione pathway gene variation and risk of autism spectrum disorders.Journal of neurodevelopmental disorders · 2011Article
- Residential proximity to freeways and autism in the CHARGE study.Environmental health perspectives · 2011Article
- The plausibility of a role for mercury in the etiology of autism: a cellular perspective.Toxicological and environmental chemistry · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundCertain loci on the human genome, such as glutathione S-transferase M1 (GSTM1), do not permit heterozygotes to be reliably determined by commonly used methods. Association of such a locus with a disease is therefore generally tested with a case-control design. When subjects have already been ascertained in a case-parent design however, the question arises as to whether the data can still be used to test disease association at such a locus.
resultsA likelihood ratio test was constructed that can be used with a case-parents design but has somewhat less power than a Pearson's chi-squared test that uses a case-control design. The test is illustrated on a novel dataset showing a genotype relative risk near 2 for the homozygous GSTM1 deletion genotype and autism.
conclusionAlthough the case-control design will remain the mainstay for a locus with a deletion, the likelihood ratio test will be useful for such a locus analyzed as part of a larger case-parent study design. The likelihood ratio test has the advantage that it can incorporate complete and incomplete case-parent trios as well as independent cases and controls. Both analyses support (p = 0.046 for the proposed test, p = 0.028 for the case-control analysis) an association of the homozygous GSTM1 deletion genotype with autism.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.