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Lack of Association of catechol‐ O ‐Methyltransferase Gene Polymorphism in Obsessive–Compulsive Disorder
Author(s) -
Erdal M. Emin,
Tot Şenel,
Yazıcı Kemal,
Yazıcı Aylin,
Herken Hasan,
Erdem Pervin,
Derici Ebru,
Çamdeviren Handan
Publication year - 2003
Publication title -
depression and anxiety
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.634
H-Index - 129
eISSN - 1520-6394
pISSN - 1091-4269
DOI - 10.1002/da.10114
Subject(s) - catechol o methyl transferase , allele , genotype , polymorphism (computer science) , genetics , gene polymorphism , family history , allele frequency , gene , medicine , biology
The COMT gene has been implicated to be involved in the pathogenesis of obsessive–compulsive disorder (OCD) and various other psychiatric disorders. COMT enzyme activity is governed by a common genetic polymorphism at codon 158 that results in substantial 3‐ to 4‐fold variation in enzymatic activity [a high‐activity COMT variant (H) and a low activity variant (L)]. This study evaluates the association between OCD and the COMT gene polymorphism. Fifty‐nine OCD patients that were diagnosed according to DSM‐IV criteria and 114 healthy control subjects were included in the study. PCR technique was used for molecular analysis. The genotypic pattern of distribution of the COMT gene (H/H, H/L, and L/L genotypes) was not different between the OCD patients and controls. There were no significant differences among the patients with positive family history for OCD, those with negative family history for OCD, and the controls with respect to allele frequencies of the COMT gene polymorphisms. Patients that were homozygous or heterozygous for the L allele had significantly higher insight scores (i.e., poorer insight) on Y‐BOCS compared to those homozygous for the H allele. We did not find an association between OCD, family history for OCD, and the COMT gene polymorphism. This study suggests that the COMT gene polymorphism is not directly associated with OCD in our patient group. Depression and Anxiety 18:41–45, 2003. © 2003 Wiley‐Liss, Inc.