Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
2566326 | Progress in Neuro-Psychopharmacology and Biological Psychiatry | 2007 | 7 Pages |
Evidence has supported a role for serotonin system dysfunction in the pathogenesis of the obsessive–compulsive disorder (OCD). Many studies examined the association between OCD and a functional polymorphism of the serotonin transporter gene promoter (5-HTTLPR) but yielded inconsistent results. Current study aimed to determine conclusively whether there is an association by using a meta-analytic method. Over 3000 subjects from 13 independent case-control association studies were included in the analysis. By using random effects model, data from these studies were pooled to compare the genotypes and allelic distribution of the 5-HTTLPR polymorphism between OCD patients and control subjects. In the analysis, OCD was found to be associated with the SS homozygous genotype (OR = 1.21, p = 0.04), but was inversely associated with the LS heterozygous genotype (OR = 0.79, p = 0.03). No association with the LL homozygous genotype or the allelic distribution was found. These results suggest that variations of the serotonin transporter gene influence the risk of OCD, but their functional roles in the pathogenesis of OCD need to be elucidated.