Tryptophan hydroxylase (TPH) is the rate-limiting enzyme in the synthesis of 5-hydroxytryptamine (5-HT). An association study in bipolar affective disorder I or unipolar major affective disorder was performed by using a Bfa I restriction site polymorphism within intron 7 of the tryptophan hydroxylas
Association of DAO and G72(DAOA)/G30 genes with bipolar affective disorder
β Scribed by Diana Prata; Gerome Breen; Sarah Osborne; Janet Munro; David St. Clair; David Collier
- Publisher
- John Wiley and Sons
- Year
- 2007
- Tongue
- English
- Weight
- 58 KB
- Volume
- 147B
- Category
- Article
- ISSN
- 1552-4841
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β¦ Synopsis
Abstract
There is growing evidence of partial aetiological overlap between schizophrenia and bipolar disorder (BP) from linkage analysis, genetic epidemiology and molecular genetics studies. In the present study we investigated whether individual polymorphisms or haplotypes of the DAO and G72(DAOA)/G30 genes, which have been previously implicated in schizophrenia, are also associated with bipolar disorder. For each gene, we genotyped 213 cases and 197 controls for SNPs previously associated with schizophrenia: rs2111902 (MDAAOβ4), rs3918346 (MDAAOβ5), rs3741775 (MDAAOβ6) and rs3918347 (MDAAOβ7) in DAO and rs746187 (M7), rs3916966 (M13), rs2391191 (M15) and rs3916972 (M25) in G72. Although none of the individual SNPs in these genes reached statistical significance, we found haplotype wise associations with bipolar disorder for both genes. These included a twoβSNP haplotype in DAO (rs2111902βA and rs3918346βT; global Pβ=β0.003, individual Pβ=β0.002, Zβ=β3.1) and a twoβSNP haplotype for G72(DAOA)/G30 (rs746187βG and rs3916972βG; global Pβ=β0.05; individual Pβ=β0.005, Zβ=β2.81). However, we found no evidence for an epistatic interaction between the SNPs and/or haplotypes of the two genes. In summary, our findings provide some support for the individual involvement of DAO and G72(DAOA)/G30 in the etiology of bipolar disorder. Β© 2007 WileyβLiss, Inc.
π SIMILAR VOLUMES
## Abstract Convincing evidence for a genetic component in the etiology of affective disorders (AD), including bipolar affective disorder (BPAD) and unipolar affective disorder (UPAD), is supported by traditional and molecular genetic studies. Most arguments lead to the complex inheritance hypothes