Association studies of serotonin system candidate genes in early-onset obsessive-compulsive disorder

被引:70
作者
Dickel, Diane E.
Veenstra-VanderWeele, Jeremy
Bivens, Nancy Chiu
Wu, Xiaolin
Fischer, Daniel J.
Van Etten-Lee, Michelle
Himle, Joseph A.
Leventhal, Bennett L.
Cook, Edwin H., Jr.
Hanna, Gregory L.
机构
[1] Univ Illinois, Dept Psychiat, Inst Juvenile Res, Chicago, IL 60612 USA
[2] Univ Chicago, Dept Med, Chicago, IL 60637 USA
[3] Univ Michigan, Dept Psychiat, Ann Arbor, MI 48109 USA
基金
美国国家卫生研究院;
关键词
genetic; obsessive-compulsive disorder; polymorphism; serotonin; tic disorder; transmission disequilibrium;
D O I
10.1016/j.biopsych.2006.09.030
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Background. Family-based evidence for association at serotonin system genes SLC6A4, HTR1B, HTR2A, and brain-derived neurotrophic factor (BDNF) has been previously reported in obsessive-compulsive disorder (OCD). Early-onset CCD is a more familial form of the disorder. Methods. We used the transmission-disequilibrium test of association at common polymorpbisms in each of these genes in 54 parent-child trios ascertained through probands with early-onset OCD. Results: No evidence for association was detected at any of the polymorpbisms in the entire set of subjects. Nominally significant association was,found at the HTR2A rs6311 polymorpbism in subjects with tic disorder and OCD (p =.05), replicating a previous finding in Tourette syndrome and OCD. Nominally significant association was also found for the SLC6A4 HT transporter gene-linked polymorphic region (5-HMPR) polymorpbism for female subjects (p =.03). Neither association would remain significant after statistical correction for multiple testing. Despite no individual study reporting replication, a pooled analysis of five replication studies of the SLC6A4 5-HTTLPR polymorphism supports association (p =.02). Conclusions. Low power across individual association studies in OCD may lead to a false acceptance of the null hypothesis. Accumulation of evidence from multiple studies will be necessary to evaluate the potential role for these genes in contributing to susceptibility to OCD.
引用
收藏
页码:322 / 329
页数:8
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