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Your search keyword '"Someya, T."' showing total 11 results
Start Over Author "Someya, T." Journal molecular psychiatry
11 results on '"Someya, T."'

1. High-resolution copy number variation analysis of schizophrenia in Japan

Author

Kushima, I, Aleksic, B, Nakatochi, M, Shimamura, T, Shiino, T, Yoshimi, A, Kimura, H, Takasaki, Y, Wang, C, Xing, J, Ishizuka, K, Oya-Ito, T, Nakamura, Y, Arioka, Y, Maeda, T, Yamamoto, M, Yoshida, M, Noma, H, Hamada, S, Morikawa, M, Uno, Y, Okada, T, Iidaka, T, Iritani, S, Yamamoto, T, Miyashita, M, Kobori, A, Arai, M, Itokawa, M, Cheng, M -C, Chuang, Y -A, Chen, C -H, Suzuki, M, Takahashi, T, Hashimoto, R, Yamamori, H, Yasuda, Y, Watanabe, Y, Nunokawa, A, Someya, T, Ikeda, M, Toyota, T, Yoshikawa, T, Numata, S, Ohmori, T, Kunimoto, S, Mori, D, Iwata, N, and Ozaki, N

Published
2017
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7. High-resolution copy number variation analysis of schizophrenia in Japan

Author

Kushima, I, primary, Aleksic, B, additional, Nakatochi, M, additional, Shimamura, T, additional, Shiino, T, additional, Yoshimi, A, additional, Kimura, H, additional, Takasaki, Y, additional, Wang, C, additional, Xing, J, additional, Ishizuka, K, additional, Oya-Ito, T, additional, Nakamura, Y, additional, Arioka, Y, additional, Maeda, T, additional, Yamamoto, M, additional, Yoshida, M, additional, Noma, H, additional, Hamada, S, additional, Morikawa, M, additional, Uno, Y, additional, Okada, T, additional, Iidaka, T, additional, Iritani, S, additional, Yamamoto, T, additional, Miyashita, M, additional, Kobori, A, additional, Arai, M, additional, Itokawa, M, additional, Cheng, M -C, additional, Chuang, Y -A, additional, Chen, C -H, additional, Suzuki, M, additional, Takahashi, T, additional, Hashimoto, R, additional, Yamamori, H, additional, Yasuda, Y, additional, Watanabe, Y, additional, Nunokawa, A, additional, Someya, T, additional, Ikeda, M, additional, Toyota, T, additional, Yoshikawa, T, additional, Numata, S, additional, Ohmori, T, additional, Kunimoto, S, additional, Mori, D, additional, Iwata, N, additional, and Ozaki, N, additional

Published
2016
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8. A genome-wide association study identifies two novel susceptibility loci and trans population polygenicity associated with bipolar disorder

Author

Ikeda, M, Takahashi, A, Kamatani, Y, Okahisa, Y, Kunugi, H, Mori, N, Sasaki, T, Ohmori, T, Okamoto, Y, Kawasaki, H, Shimodera, S, Kato, T, Yoneda, H, Yoshimura, R, Iyo, M, Matsuda, K, Akiyama, M, Ashikawa, K, Kashiwase, K, Tokunaga, K, Kondo, K, Saito, T, Shimasaki, A, Kawase, K, Kitajima, T, Matsuo, K, Itokawa, M, Someya, T, Inada, T, Hashimoto, R, Inoue, T, Akiyama, K, Tanii, H, Arai, H, Kanba, S, Ozaki, N, Kusumi, I, Yoshikawa, T, Kubo, M, and Iwata, N

Abstract

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 (Pbest=5.8 × 10−10), and supported three regions previously implicated in BD susceptibility: MAD1L1 (Pbest=1.9 × 10−9), TRANK1 (Pbest=2.1 × 10−9) and ODZ4 (Pbest=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.

Published
2018
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9. Genetic evidence for association between NOTCH4 and schizophrenia supported by a GWAS follow-up study in a Japanese population

Author

Ikeda, M, primary, Aleksic, B, additional, Yamada, K, additional, Iwayama-Shigeno, Y, additional, Matsuo, K, additional, Numata, S, additional, Watanabe, Y, additional, Ohnuma, T, additional, Kaneko, T, additional, Fukuo, Y, additional, Okochi, T, additional, Toyota, T, additional, Hattori, E, additional, Shimodera, S, additional, Itakura, M, additional, Nunokawa, A, additional, Shibata, N, additional, Tanaka, H, additional, Yoneda, H, additional, Arai, H, additional, Someya, T, additional, Ohmori, T, additional, Yoshikawa, T, additional, Ozaki, N, additional, and Iwata, N, additional

Published
2012
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11. Deep exome sequencing identifies enrichment of deleterious mosaic variants in neurodevelopmental disorder genes and mitochondrial tRNA regions in bipolar disorder.

Author

Nishioka M, Takayama J, Sakai N, Kazuno AA, Ishiwata M, Ueda J, Hayama T, Fujii K, Someya T, Kuriyama S, Tamiya G, Takata A, and Kato T

Subjects
Humans, Genetic Predisposition to Disease genetics, Exome Sequencing, Bipolar Disorder genetics, Autism Spectrum Disorder genetics, Mitochondrial Diseases
Abstract

Bipolar disorder (BD) is a global medical issue, afflicting around 1% of the population with manic and depressive episodes. Despite various genetic studies, the genetic architecture and pathogenesis of BD have not been fully resolved. Besides germline variants, postzygotic mosaic variants are proposed as new candidate mechanisms contributing to BD. Here, we performed extensive deep exome sequencing (DES, ~300×) and validation experiments to investigate the roles of mosaic variants in BD with 235 BD cases (194 probands of trios and 41 single cases) and 39 controls. We found an enrichment of developmental disorder (DD) genes in the genes hit by deleterious mosaic variants in BD (P = 0.000552), including a ClinVar-registered pathogenic variant in ARID2. An enrichment of deleterious mosaic variants was also observed for autism spectrum disorder (ASD) genes (P = 0.000428). The proteins coded by the DD/ASD genes with non-synonymous mosaic variants in BD form more protein-protein interaction than expected, suggesting molecular mechanisms shared with DD/ASD but restricted to a subset of cells in BD. We also found significant enrichment of mitochondrial heteroplasmic variants, another class of mosaic variants, in mitochondrial tRNA genes in BD (P = 0.0102). Among them, recurrent m.3243 A > G variants known as causal for mitochondrial diseases were found in two unrelated BD probands with allele fractions of 5-12%, lower than in mitochondrial diseases. Despite the limitation of using peripheral tissues, our DES investigation supports the possible contribution of deleterious mosaic variants in the nuclear genome responsible for severer phenotypes, such as DD/ASD, to the risk of BD and further demonstrates that the same paradigm can be applied to the mitochondrial genome. These results, as well as the enrichment of heteroplasmic mitochondrial tRNA variants in BD, add a new piece to the understanding of the genetic architecture of BD and provide general insights into the pathological roles of mosaic variants in human diseases., (© 2023. The Author(s).)

Published
2023
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