期刊
PSYCHIATRIC GENETICS
卷 17, 期 2, 页码 109-112出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/YPG.0b013e328012a0c6
关键词
association; attention deficit hyperactivity disorder; gene; genetics; synapsin III
Objective: Recent studies have implicated the involvement of proteins regulating neurotransmitter release in the etiology of attention deficit hyperactivity disorder. On the basis of the role of synapsin III in the modulation of neurotransmitter release, we tested this gene as a candidate contributing to the genetic susceptibility of attention deficit hyperactivity disorder. Method: In this study, we genotyped five markers across the gene on 177 small, nuclear families consisting of an attention deficit hyperactivity disorder proband, their parents, and 43 affected siblings. We examined the transmission of the alleles at each one of these sites and the haplotypes of the polymorphisms using the transmission disequilibrium test. Result: Our observations did not yield any evidence of biased transmission of the alleles at any polymorphism or haplotype. On the basis of the evidence for synapsins in learning and memory from animal models, we also investigated the relationship of this gene to verbal short-term and working memory as measured by digit span forward and backwards. No evidence was found for an association of this gene to these traits. Conclusion: Our findings with this particular sample do not support the synapsin III locus as a major susceptibility locus contributing to attention deficit hyperactivity disorder.
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