2002 Fiscal Year Final Research Report Summary
Association studies with internal control for candidate genes of bipolar disorders
| Project/Area Number |
12670933
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Psychiatric science
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| Research Institution | University of Yamanashi Faculty of Medicine |
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Principal Investigator |
HIRANO Masami University of Yamanashi, Faculty of Medicine, Assistant Professor, 医学部, 講師 (80228808)
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| Co-Investigator(Kenkyū-buntansha) |
SHINOHARA Manabu University of Yamanashi, Faculty of Medicine, Research Associate, 医学部, 助手 (30273048)
SHIOE Kunihiko University of Yamanashi, Faculty of Medicine, Assistant Professor, 医学部, 講師 (90215939)
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| Project Period (FY) |
2000 – 2002
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| Keywords | bipolar disorders / candidate gene / PDE9A / TRPM2 / haplotype analysis / personality trait / TCI |
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| Research Abstract |
1. PDE9A gene and TRPM2 gene were mapped in the neighborhood of PFKL on human chromosome 21q22.3, which was a candidate region for bipolar disorder.
We have identified several single nucleotide polymorphisms. Then, using of haplotype analysis, we performed an association study of bipolar patients related to these candidate genes. There was no association observed in the present study between bipolar disorder and these newly defined polymorphisms.
2. We tested the Cloninger's four-factor model of personality structure in a Japanese twin sample, to verified the contribution of genetic and environment. Among four temperament dimensions (novelty seeking : NS, harm avoidance : HA, reward dependence : RD and persistence : PS), multivariate genetic analysis indicated that there were no significant associations between NS, HA, and RD. NS and RD could be explained by either genetic or shared environmental factors with nonshared environment. HA and PS showed significant additive genetic contributions and no shared environmental effect. Although most of the nonshared environmental effects were trait-specific, the phenotypic correlation between NS and HA could be explained by nonshared environmental overlap.
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