Preliminary genomewide association study of bipolar disorder in the Japanese populationHow to Cite this Article: Hattori E, Toyota T, Ishitsuka Y, Iwayama Y, Yamada K, Ujike H, Morita Y, Kodama M, Nakata K, Minabe Y, Nakamura K, Iwata Y, Takei N, Mori N, Naitoh H, Yamanouchi Y, Iwata N, Ozaki N, Kato T, Nishikawa T, Kashiwa A, Suzuki M, Shioe K, Shinohara M, Hirano M, Nanko S, Akahane A, Ueno M, Kaneko N, Watanabe Y, Someya T, Hashimoto K, Iyo M, Itokawa M, Arai M, Nankai M, Inada T, Yoshida S, Kunugi H, Nakamura M, Iijima Y, Okazaki Y, Higuchi T, Yoshikawa T. 2009. Preliminary GenomeWide Association Study of Bipolar Disorder in the Japanese Population. Am J Med Genet Part B 150B:1110–1117.

Autor: Hattori, Eiji, Toyota, Tomoko, Ishitsuka, Yuichi, Iwayama, Yoshimi, Yamada, Kazuo, Ujike, Hiroshi, Morita, Yukitaka, Kodama, Masafumi, Nakata, Kenji, Minabe, Yoshio, Nakamura, Kazuhiko, Iwata, Yasuhide, Takei, Nori, Mori, Norio, Naitoh, Hiroshi, Yamanouchi, Yoshio, Iwata, Nakao, Ozaki, Norio, Kato, Tadafumi, Nishikawa, Toru, Kashiwa, Atsushi, Suzuki, Mika, Shioe, Kunihiko, Shinohara, Manabu, Hirano, Masami, Nanko, Shinichiro, Akahane, Akihisa, Ueno, Mikako, Kaneko, Naoshi, Watanabe, Yuichiro, Someya, Toshiyuki, Hashimoto, Kenji, Iyo, Masaomi, Itokawa, Masanari, Arai, Makoto, Nankai, Masahiro, Inada, Toshiya, Yoshida, Sumiko, Kunugi, Hiroshi, Nakamura, Michiko, Iijima, Yoshimi, Okazaki, Yuji, Higuchi, Teruhiko, Yoshikawa, Takeo
Zdroj: American Journal of Medical Genetics. Part B, Neuropsychiatric Genetics: The Official Publication of the International Society of Psychiatric Genetics; December 2009, Vol. 150 Issue: 8 p1110-1117, 8p
Abstrakt: Recent progress in genotyping technology and the development of public databases has enabled largescale genomewide association tests with diseases. We performed a twostage genomewide 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 followup 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 twostage analysis, 89 markers remained nominally significant allelic P < 0.05 with the same allele being consistently overrepresented in both the first and the followup stages. However, none of these were significant after correction for multipletesting 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 WileyLiss, Inc.
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