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ID 115603
タイトル別表記
GWAS of bipolar disorder
著者
Ikeda, M Fujita Health University
Takahashi, A RIKEN Center for Integrative Medical Sciences|National Cerebral and Cardiovascular Center
Kamatani, Y RIKEN Center for Integrative Medical Sciences
Okahisa, Y Okayama University
Kunugi, H National Center of Neurology and Psychiatry
Mori, N Hamamatsu University School of Medicine
Sasaki, T The University of Tokyo
大森, 哲郎 The University of Tokushima KAKEN研究者をさがす
Okamoto, Y Hiroshima University
Kawasaki, H Fukuoka University
Shimodera, S Kochi University
Kato, T RIKEN Brain Science Institute
Yoneda, H Osaka Medical College
Yoshimura, R University of Occupational and Environmental Health
Iyo, M Chiba University
Matsuda, K The University of Tokyo
Akiyama, M RIKEN Center for Integrative Medical Sciences
Ashikawa, K RIKEN
Kashiwase, K Japanese Red Cross Kanto-Koshinetsu Block Blood Center
Tokunaga, K University of Tokyo
Kondo, K Fujita Health University
Saito, T Fujita Health University
Shimasaki, A Fujita Health University
Kawase, K Fujita Health University
Kitajima, T Fujita Health University
Matsuo, K Yamaguchi University
Itokawa, M Tokyo Metropolitan Institute of Medical Science
Someya, T Niigata University
Inada, T Nagoya University
Hashimoto, R Osaka University
Inoue, T Tokyo Medical University
Akiyama, K Dokkyo Medical University
Tanii, H Mie University
Arai, H Juntendo University
Kanba, S Kyushu University
Ozaki, N Nagoya University
Kusumi, I Hokkaido University
Yoshikawa, T RIKEN Brain Science Institute
Kubo, M RIKEN Center for Integrative Medical Sciences
Iwata, N Fujita Health University
資料タイプ
学術雑誌論文
抄録
Genome-wide association studies (GWASs) have identified several susceptibility loci for bipolar disorder (BD) and shown that the genetic architecture of BD can be explained by polygenicity, with numerous variants contributing to BD. In the present GWAS (Phase I/II), which included 2964 BD and 61 887 control subjects from the Japanese population, we detected a novel susceptibility locus at 11q12.2 (rs28456, P=6.4 × 10−9), a region known to contain regulatory genes for plasma lipid levels (FADS1/2/3). A subsequent meta-analysis of Phase I/II and the Psychiatric GWAS Consortium for BD (PGC-BD) identified another novel BD gene, NFIX (P best=5.8 × 10−10), and supported three regions previously implicated in BD susceptibility: MAD1L1 (P best=1.9 × 10−9), TRANK1 (P best=2.1 × 10−9) and ODZ4 (P best=3.3 × 10−9). Polygenicity of BD within Japanese and trans-European-Japanese populations was assessed with risk profile score analysis. We detected higher scores in BD cases both within (Phase I/II) and across populations (Phase I/II and PGC-BD). These were defined by (1) Phase II as discovery and Phase I as target, or vice versa (for ‘within Japanese comparisons’, Pbest~10−29, R2~2%), and (2) European PGC-BD as discovery and Japanese BD (Phase I/II) as target (for ‘trans-European-Japanese comparison,’ Pbest~10−13, R2~0.27%). This ‘trans population’ effect was supported by estimation of the genetic correlation using the effect size based on each population (liability estimates~0.7). These results indicate that (1) two novel and three previously implicated loci are significantly associated with BD and that (2) BD ‘risk’ effect are shared between Japanese and European populations.
掲載誌名
Molecular Psychiatry
ISSN
13594184
14765578
cat書誌ID
AA11164978
AA12909982
出版者
Springer Nature
23
3
開始ページ
639
終了ページ
647
発行日
2017-01-24
権利情報
This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-sa/4.0/
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出版社版DOI
出版社版URL
フルテキストファイル
言語
eng
著者版フラグ
出版社版
部局
医学系