ArticleJournal of molecular neuroscience : MN2017
Synaptosome-Associated Protein 25 (SNAP25) Gene Association Analysis Revealed Risk Variants for ASD, in Iranian Population.
Article in Journal of molecular neuroscience : MN, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 25 citations in OpenAlex.
- The Genetic Landscape of Autism in Iran: A Systematic Review.Iranian journal of psychiatry · 2026Review
- Long read whole genome sequencing-based discovery of structural variants and their role in aetiology of non-syndromic autism spectrum disorder in India.BMC medical genomics · 2025Article
- Article
- The Role ofInternational journal of molecular sciences · 2023Article
- Nexus between genome-wide copy number variations and autism spectrum disorder in Northeast Han Chinese population.BMC psychiatry · 2023Article
- Protein Misfolding and Aggregation in the Brain: Common Pathogenetic Pathways in Neurodegenerative and Mental Disorders.International journal of molecular sciences · 2022Review
- Genetic and molecular biology of autism spectrum disorder among Middle East population: a review.Human genomics · 2021Review
- An altered glial phenotype in the NL3Scientific reports · 2020Article
- Changes in the Expression of SNAP-25 Protein in the Brain of Juvenile Rats in Two Models of Autism.Journal of molecular neuroscience : MN · 2020Article
- Prenatal Exposure to Valproic Acid Affects Microglia and Synaptic Ultrastructure in a Brain-Region-Specific Manner in Young-Adult Male Rats: Relevance to Autism Spectrum Disorders.International journal of molecular sciences · 2020Article
- Reduced SNAP25 Protein Fragmentation Contributes to SNARE Complex Dysregulation in Schizophrenia Postmortem Brain.Neuroscience · 2019Article
- Application of Single-Nucleotide Polymorphisms in the Diagnosis of Autism Spectrum Disorders: A Preliminary Study with Artificial Neural Networks.Journal of molecular neuroscience : MN · 2019Article
- Sex-Specific Proteomic Changes Induced by Genetic Deletion of Fibroblast Growth Factor 14 (FGF14), a Regulator of Neuronal Ion Channels.Proteomes · 2019Article
- Ras-like without CAAX 2 (RIT2): a susceptibility gene for autism spectrum disorder.Metabolic brain disease · 2017Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autism spectrum disorder (ASD) is a common, complex neurological condition, affecting approximately 1% of people worldwide. Monogenic neurodevelopmental disorders which showed autistic behavior patterns have suggested synaptic dysfunction, as a key mechanism in the pathophysiology of ASD. Subsequently, genes involved in synaptic signaling have been investigated with a priority for candidate gene studies. A synaptosomal-associated protein 25 (SNAP25) gene plays a crucial role in the central nervous system, contributing to exocytosis by targeting and fusion of vesicles to the cell membrane. Studies have shown a correlation between aberrant expression of the SNAP25 and a variety of brain diseases. Single nucleotide polymorphisms (SNPs) in this gene are associated with several psychiatric diseases, such as bipolar, schizophrenia, and attention-deficit/hyperactivity disorder. The aim of the present study was to investigate whether polymorphisms (rs3746544 and rs1051312) in the regulatory 3'-untranslated region (3'UTR) of the SNAP25 gene have an association with ASD in unrelated Iranian case (N = 524)-control (N = 472) samples. We observed robust association of the rs3746544 SNP and ASD patients, in both allele and haplotype-based analyses. Our results supported the previous observations and indicated a possible role for SNAP25 polymorphisms as susceptibility genetic factors involved in developing ASD.
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