ArticleEuropean archives of psychiatry and clinical neuroscience2019
STX1A gene variations contribute to the susceptibility of children attention-deficit/hyperactivity disorder: a case-control association study.
Article in European archives of psychiatry and clinical neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 13 citations in OpenAlex.
- Syntaxin1A in synaptopathies: From molecular mechanisms to therapeutic implications in neurological disorders (Review).Biomedical reports · 2026Review
- Circadian clock crosstalks with autism.Brain and behavior · 2023Article
- Methamphetamine-induced region-specific transcriptomic and epigenetic changes in the brain of male rats.Communications biology · 2023Article
- Heterozygous and homozygous variants in STX1A cause a neurodevelopmental disorder with or without epilepsy.European journal of human genetics : EJHG · 2023Article
- Dehydroepiandrosterone alleviates hypoxia-induced learning and memory dysfunction by maintaining synaptic homeostasis.CNS neuroscience & therapeutics · 2022Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
It was presumed syntaxin-1A (STX1A) might relate to the pathophysiology of attention-deficit/hyperactivity disorder (ADHD), but the results were inconsistent. The present study aims to confirm whether the STX1A gene is involved in the susceptibility of children ADHD. We genotyped three single nucleotide polymorphisms (SNPs) of STX1A gene using Sequenom MassARRAY technology. A case-control study was performed among Chinese Han population including 754 cases and 772 controls from two different provinces. The Conners Parent Symptom Questionnaire and Integrated Visual and Auditory Continuous Performance Test were used to assess ADHD clinical symptoms. We found for the first time that rs3793243 GG genotype carriers had a lower risk of ADHD compared with AA genotype (OR 0.564, 95% confidence interval (CI) 0.406-0.692, P = 0.001), and rs875342 was also associated with children ADHD (OR 1.806, 95% CI 1.349-2.591, P = 0.001). In addition, the two positive SNPs were also significantly associated with the clinical characteristics of ADHD. Expression quantitative trait loci analysis indicated that rs3793243 might mediate STX1A gene expression. Using a case-control study to explore the association between STX1A gene and children ADHD in Chinese Han population, our results suggest STX1A genetic variants might contribute to the susceptibility of children ADHD.
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