Association between 1603C>T polymorphism of DBH gene and bipolar disorder in a Turkish population

Dopamine-β-hydroxylase (DBH) is the enzyme responsible for the conversion of dopamine (DA) to norepinephrine (NE, noradrenaline) which is a key neurotransmitter in the central and peripheral nervous systems. Bipolar disorder is a major psychiatric disorder. The present study was designed to explore...

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Published inGene Vol. 519; no. 2; pp. 356 - 359
Main Authors Ates, Omer, Celikel, Feryal Cam, Taycan, Serap Erdogan, Sezer, Saime, Karakus, Nevin
Format Journal Article
LanguageEnglish
Published Netherlands Elsevier B.V 01.05.2013
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Summary:Dopamine-β-hydroxylase (DBH) is the enzyme responsible for the conversion of dopamine (DA) to norepinephrine (NE, noradrenaline) which is a key neurotransmitter in the central and peripheral nervous systems. Bipolar disorder is a major psychiatric disorder. The present study was designed to explore the associations of polymorphisms of DBH gene in Turkish patients with bipolar disorder. −1021C>T (rs1611115) polymorphism in promoter region, 444G>A (rs1108580) polymorphism in exon 2 and 1603C>T (rs6271; C535R) polymorphism in exon11 of DBH gene were analyzed in 106 patients with bipolar disorder and 106 healthy subjects by using polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP) analysis. The results showed statistically significant associations for genotypic and allelic distribution between the 1603C>T polymorphism and bipolar disease (p=0.0012 and p=0.034, respectively). There was no association observed between the genotype and allelic frequencies for −1021C>T and 444G>A polymorphisms and bipolar disorder. Our data suggests that the 1603C>T polymorphism of the DBH gene is associated with susceptibility to bipolar disorder in a Turkish population. ► Decreased DBH plasma activity was observed in patients with bipolar disorder. ► 1603C>T polymorphism is associated with susceptibility to bipolar disorder. ► −1021C>T and 444G>A polymorphisms are not associated with bipolar disorder.
Bibliography:http://dx.doi.org/10.1016/j.gene.2013.01.031
ObjectType-Article-1
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ISSN:0378-1119
1879-0038
1879-0038
DOI:10.1016/j.gene.2013.01.031