Literature DB >> 19259986

Preliminary genome-wide association study of bipolar disorder in the Japanese population.

Eiji Hattori1, Tomoko Toyota, Yuichi Ishitsuka, Yoshimi Iwayama, Kazuo Yamada, Hiroshi Ujike, Yukitaka Morita, Masafumi Kodama, Kenji Nakata, Yoshio Minabe, Kazuhiko Nakamura, Yasuhide Iwata, Nori Takei, Norio Mori, Hiroshi Naitoh, Yoshio Yamanouchi, Nakao Iwata, Norio Ozaki, Tadafumi Kato, Toru Nishikawa, Atsushi Kashiwa, Mika Suzuki, Kunihiko Shioe, Manabu Shinohara, Masami Hirano, Shinichiro Nanko, Akihisa Akahane, Mikako Ueno, Naoshi Kaneko, Yuichiro Watanabe, Toshiyuki Someya, Kenji Hashimoto, Masaomi Iyo, Masanari Itokawa, Makoto Arai, Masahiro Nankai, Toshiya Inada, Sumiko Yoshida, Hiroshi Kunugi, Michiko Nakamura, Yoshimi Iijima, Yuji Okazaki, Teruhiko Higuchi, Takeo Yoshikawa.   

Abstract

Recent progress in genotyping technology and the development of public databases has enabled large-scale genome-wide association tests with diseases. We performed a two-stage genome-wide association study (GWAS) of bipolar disorder (BD) in Japanese cohorts. First we used Affymetrix 100K GeneChip arrays in the analysis of 107 cases with bipolar I disorder and 107 controls, and selected markers that were nominally significant (P < 0.01) in at least one of the three models (1,577 markers in total). In the follow-up stage, we analyzed these markers using an Illumina platform (1,526 markers; 51 markers were not designable for the platform) and an independent sample set, which consisted of 395 cases (bipolar I + II) and 409 controls. We also assessed the population stratification of current samples using principal components analysis. After the two-stage analysis, 89 markers remained nominally significant (allelic P < 0.05) with the same allele being consistently over-represented in both the first and the follow-up stages. However, none of these were significant after correction for multiple-testing by false discovery rates. Sample stratification was virtually negligible. Collectively, this is the first GWAS of BD in the Japanese population. But given the small sample size and the limited genomic coverage, these results should be taken as preliminary. 2009 Wiley-Liss, Inc.

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Year:  2009        PMID: 19259986     DOI: 10.1002/ajmg.b.30941

Source DB:  PubMed          Journal:  Am J Med Genet B Neuropsychiatr Genet        ISSN: 1552-4841            Impact factor:   3.568


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