ArticleJournal of neural transmission (Vienna, Austria : 1996)2009
A population-based association study of glutamate decarboxylase 1 as a candidate gene for autism.
Article in Journal of neural transmission (Vienna, Austria : 1996), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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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
10 citing papers in PubMed, 14 citations in OpenAlex.
- Trial
- Modulating autism spectrum disorder pathophysiology using a trace amine-focused approach: targeting the gut.Molecular medicine (Cambridge, Mass.) · 2025Review
- Molecular underpinnings of prefrontal cortex development in rodents provide insights into the etiology of neurodevelopmental disorders.Molecular psychiatry · 2015Review
- Developing Medications Targeting Glutamatergic Dysfunction in Autism: Progress to Date.CNS drugs · 2015Review
- Disturbed cingulate glutamate metabolism in adults with high-functioning autism spectrum disorder: evidence in support of the excitatory/inhibitory imbalance hypothesis.Molecular psychiatry · 2014Article
- Impairment of cortical GABAergic synaptic transmission in an environmental rat model of autism.The international journal of neuropsychopharmacology · 2013Article
- Gender differences in associations of glutamate decarboxylase 1 gene (GAD1) variants with panic disorder.PloS one · 2012Article
- Common genetic variation in the GAD1 gene and the entire family of DLX homeobox genes and autism spectrum disorders.American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics · 2011Article
- Validity of childhood autism in the Danish Psychiatric Central Register: findings from a cohort sample born 1990-1999.Journal of autism and developmental disorders · 2010Article
- Syndromic autism: causes and pathogenetic pathways.World journal of pediatrics : WJP · 2009Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Linkage studies, genome-wide scans and screening of possible candidate genes suggest that chromosome 2q31 may harbour one or more susceptibility genes for autism. The glutamate decarboxylase gene 1 (GAD1) located within chromosome 2q31 encodes the enzyme, GAD67, catalyzing the production of gamma-aminobutyric acid (GABA) from glutamate. Numerous independent findings have suggested the GABAergic system to be involved in autism. The present study investigates a Danish population-based, case-control sample of 444 subjects with childhood autism and 444 controls. Nine single nucleotide polymorphisms (SNPs) comprising the GAD1 gene and the microsatellite marker D2S2381 were examined for association with autism. We found no association between childhood autism and any single marker or 2-5 marker haplotypes. However, a rare nine-marker haplotype was associated with childhood autism. We cannot exclude neither GAD1 as a susceptibility gene nor the possibility of another susceptibility gene for autism to be located on chromosome 2q31.
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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.