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1. Exome sequencing analysis of Japanese autism spectrum disorder case-control sample supports an increased burden of synaptic function-related genes

Author

Kimura, Hiroki, Nakatochi, Masahiro, Aleksic, Branko, Guevara, James, Toyama, Miho, Hayashi, Yu, Kato, Hidekazu, Kushima, Itaru, Morikawa, Mako, Ishizuka, Kanako, Okada, Takashi, Tsurusaki, Yoshinori, Fujita, Atsushi, Miyake, Noriko, Ogi, Tomoo, Takata, Atsushi, Matsumoto, Naomichi, Buxbaum, Joseph, Ozaki, Norio, and Sebat, Jonathan

Published
2022
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3. Did kindergarteners who experienced the Great East Japan earthquake as infants develop traumatic symptoms? Series of questionnaire-based cross-sectional surveys: A concise and informative title: traumatic symptoms of kindergarteners who experienced disasters as infants

Author

Usami, Masahide, Iwadare, Yoshitaka, Ushijima, Hirokage, Inazaki, Kumi, Tanaka, Tetsuya, Kodaira, Masaki, Watanabe, Kyota, Kawahara, Kazuhiro, Morikawa, Mako, Kontani, Keiko, Murakami, Kanako, Ogata, Remie, Okamoto, Seiko, Sekine, Keisuke, Sato, Masako, Sasaki, Yoshinori, Tanaka, Hiromi, Harada, Maiko, Imagi, Sonoko, Matsuda, Kumi, Katsumi, Chiaki, Aoki, Momoko, Makino, Kazunori, and Saito, Kazuhiko

Published
2019
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6. Rare single-nucleotide DAB1 variants and their contribution to Schizophrenia and autism spectrum disorder susceptibility

Author

Nawa, Yoshihiro, Kimura, Hiroki, Mori, Daisuke, Kato, Hidekazu, Toyama, Miho, Furuta, Sho, Yu, Yanjie, Ishizuka, Kanako, Kushima, Itaru, Aleksic, Branko, Arioka, Yuko, Morikawa, Mako, Okada, Takashi, Inada, Toshiya, Kaibuchi, Kozo, Ikeda, Masashi, Iwata, Nakao, Suzuki, Michio, Okahisa, Yuko, Egawa, Jun, Someya, Toshiyuki, Nishimura, Fumichika, Sasaki, Tsukasa, and Ozaki, Norio

Published
2020
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7. Rare genetic variants in the gene encoding histone lysine demethylase 4C (KDM4C) and their contributions to susceptibility to schizophrenia and autism spectrum disorder

Author

Kato, Hidekazu, Kushima, Itaru, Mori, Daisuke, Yoshimi, Akira, Aleksic, Branko, Nawa, Yoshihiro, Toyama, Miho, Furuta, Sho, Yu, Yanjie, Ishizuka, Kanako, Kimura, Hiroki, Arioka, Yuko, Tsujimura, Keita, Morikawa, Mako, Okada, Takashi, Inada, Toshiya, Nakatochi, Masahiro, Shinjo, Keiko, Kondo, Yutaka, Kaibuchi, Kozo, Funabiki, Yasuko, Kimura, Ryo, Suzuki, Toshimitsu, Yamakawa, Kazuhiro, Ikeda, Masashi, Iwata, Nakao, Takahashi, Tsutomu, Suzuki, Michio, Okahisa, Yuko, Takaki, Manabu, Egawa, Jun, Someya, Toshiyuki, and Ozaki, Norio

Published
2020
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10. Molecular diagnosis of 405 individuals with autism spectrum disorder

Author

Miyake, Noriko, primary, Tsurusaki, Yoshinori, additional, Fukai, Ryoko, additional, Kushima, Itaru, additional, Okamoto, Nobuhiko, additional, Ohashi, Kei, additional, Nakamura, Kazuhiko, additional, Hashimoto, Ryota, additional, Hiraki, Yoko, additional, Son, Shuraku, additional, Kato, Mitsuhiro, additional, Sakai, Yasunari, additional, Osaka, Hitoshi, additional, Deguchi, Kimiko, additional, Matsuishi, Toyojiro, additional, Takeshita, Saoko, additional, Fattal-Valevski, Aviva, additional, Ekhilevitch, Nina, additional, Tohyama, Jun, additional, Yap, Patrick, additional, Keng, Wee Teik, additional, Kobayashi, Hiroshi, additional, Takubo, Keiyo, additional, Okada, Takashi, additional, Saitoh, Shinji, additional, Yasuda, Yuka, additional, Murai, Toshiya, additional, Nakamura, Kazuyuki, additional, Ohga, Shouichi, additional, Matsumoto, Ayumi, additional, Inoue, Ken, additional, Saikusa, Tomoko, additional, Hershkovitz, Tova, additional, Kobayashi, Yu, additional, Morikawa, Mako, additional, Ito, Aiko, additional, Hara, Toshiro, additional, Uno, Yota, additional, Seiwa, Chizuru, additional, Ishizuka, Kanako, additional, Shirahata, Emi, additional, Fujita, Atsushi, additional, Koshimizu, Eriko, additional, Miyatake, Satoko, additional, Takata, Atsushi, additional, Mizuguchi, Takeshi, additional, Ozaki, Norio, additional, and Matsumoto, Naomichi, additional

Published
2023
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11. Molecular diagnosis of 405 individuals with autism spectrum disorder

Author

Miyake, Noriko, Tsurusaki, Yoshinori, Fukai, Ryoko, Kushima, Itaru, Okamoto, Nobuhiko, Ohashi, Kei, Nakamura, Kazuhiko, Hashimoto, Ryota, Hiraki, Yoko, Son, Shuraku, Kato, Mitsuhiro, Sakai, Yasunari, Osaka, Hitoshi, Deguchi, Kimiko, Matsuishi, Toyojiro, Takeshita, Saoko, Fattal-Valevski, Aviva, Ekhilevitch, Nina, Tohyama, Jun, Yap, Patrick, Keng, Wee Teik, Kobayashi, Hiroshi, Takubo, Keiyo, Okada, Takashi, Saitoh, Shinji, Yasuda, Yuka, Murai, Toshiya, Nakamura, Kazuyuki, Ohga, Shouichi, Matsumoto, Ayumi, Inoue, Ken, Saikusa, Tomoko, Hershkovitz, Tova, Kobayashi, Yu, Morikawa, Mako, Ito, Aiko, Hara, Toshiro, Uno, Yota, Seiwa, Chizuru, Ishizuka, Kanako, Shirahata, Emi, Fujita, Atsushi, Koshimizu, Eriko, Miyatake, Satoko, Takata, Atsushi, Mizuguchi, Takeshi, Ozaki, Norio, and Matsumoto, Naomichi

Abstract

Autism spectrum disorder (ASD) is caused by combined genetic and environmental factors. Genetic heritability in ASD is estimated as 60–90%, and genetic investigations have revealed many monogenic factors. We analyzed 405 patients with ASD using family-based exome sequencing to detect disease-causing single-nucleotide variants (SNVs), small insertions and deletions (indels), and copy number variations (CNVs) for molecular diagnoses. All candidate variants were validated by Sanger sequencing or quantitative polymerase chain reaction and were evaluated using the American College of Medical Genetics and Genomics/Association for Molecular Pathology guidelines for molecular diagnosis. We identified 55 disease-causing SNVs/indels in 53 affected individuals and 13 disease-causing CNVs in 13 affected individuals, achieving a molecular diagnosis in 66 of 405 affected individuals (16.3%). Among the 55 disease-causing SNVs/indels, 51 occurred de novo, 2 were compound heterozygous (in one patient), and 2 were X-linked hemizygous variants inherited from unaffected mothers. The molecular diagnosis rate in females was significantly higher than that in males. We analyzed affected sibling cases of 24 quads and 2 quintets, but only one pair of siblings shared an identical pathogenic variant. Notably, there was a higher molecular diagnostic rate in simplex cases than in multiplex families. Our simulation indicated that the diagnostic yield is increasing by 0.63% (range 0–2.5%) per year. Based on our simple simulation, diagnostic yield is improving over time. Thus, periodical reevaluation of ES data should be strongly encouraged in undiagnosed ASD patients.

Published
2024
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14. Cross-Disorder Analysis of Genic and Regulatory Copy Number Variations in Bipolar Disorder, Schizophrenia, and Autism Spectrum Disorder

Author

Kushima, Itaru, primary, Nakatochi, Masahiro, additional, Aleksic, Branko, additional, Okada, Takashi, additional, Kimura, Hiroki, additional, Kato, Hidekazu, additional, Morikawa, Mako, additional, Inada, Toshiya, additional, Ishizuka, Kanako, additional, Torii, Youta, additional, Nakamura, Yukako, additional, Tanaka, Satoshi, additional, Imaeda, Miho, additional, Takahashi, Nagahide, additional, Yamamoto, Maeri, additional, Iwamoto, Kunihiro, additional, Nawa, Yoshihiro, additional, Ogawa, Nanayo, additional, Iritani, Shuji, additional, Hayashi, Yu, additional, Lo, Tzuyao, additional, Otgonbayar, Gantsooj, additional, Furuta, Sho, additional, Iwata, Nakao, additional, Ikeda, Masashi, additional, Saito, Takeo, additional, Ninomiya, Kohei, additional, Okochi, Tomo, additional, Hashimoto, Ryota, additional, Yamamori, Hidenaga, additional, Yasuda, Yuka, additional, Fujimoto, Michiko, additional, Miura, Kenichiro, additional, Itokawa, Masanari, additional, Arai, Makoto, additional, Miyashita, Mitsuhiro, additional, Toriumi, Kazuya, additional, Ohi, Kazutaka, additional, Shioiri, Toshiki, additional, Kitaichi, Kiyoyuki, additional, Someya, Toshiyuki, additional, Watanabe, Yuichiro, additional, Egawa, Jun, additional, Takahashi, Tsutomu, additional, Suzuki, Michio, additional, Sasaki, Tsukasa, additional, Tochigi, Mamoru, additional, Nishimura, Fumichika, additional, Yamasue, Hidenori, additional, Kuwabara, Hitoshi, additional, Wakuda, Tomoyasu, additional, Kato, Takahiro A., additional, Kanba, Shigenobu, additional, Horikawa, Hideki, additional, Usami, Masahide, additional, Kodaira, Masaki, additional, Watanabe, Kyota, additional, Yoshikawa, Takeo, additional, Toyota, Tomoko, additional, Yokoyama, Shigeru, additional, Munesue, Toshio, additional, Kimura, Ryo, additional, Funabiki, Yasuko, additional, Kosaka, Hirotaka, additional, Jung, Minyoung, additional, Kasai, Kiyoto, additional, Ikegame, Tempei, additional, Jinde, Seiichiro, additional, Numata, Shusuke, additional, Kinoshita, Makoto, additional, Kato, Tadafumi, additional, Kakiuchi, Chihiro, additional, Yamakawa, Kazuhiro, additional, Suzuki, Toshimitsu, additional, Hashimoto, Naoki, additional, Ishikawa, Shuhei, additional, Yamagata, Bun, additional, Nio, Shintaro, additional, Murai, Toshiya, additional, Son, Shuraku, additional, Kunii, Yasuto, additional, Yabe, Hirooki, additional, Inagaki, Masumi, additional, Goto, Yu-ichi, additional, Okumura, Yuto, additional, Ito, Tomoya, additional, Arioka, Yuko, additional, Mori, Daisuke, additional, and Ozaki, Norio, additional

Published
2022
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16. Rare loss of function mutations in N-methyl-d-aspartate glutamate receptors and their contributions to schizophrenia susceptibility

Author

Yu, Yanjie, Lin, Yingni, Takasaki, Yuto, Wang, Chenyao, Kimura, Hiroki, Xing, Jingrui, Ishizuka, Kanako, Toyama, Miho, Kushima, Itaru, Mori, Daisuke, Arioka, Yuko, Uno, Yota, Shiino, Tomoko, Nakamura, Yukako, Okada, Takashi, Morikawa, Mako, Ikeda, Masashi, Iwata, Nakao, Okahisa, Yuko, Takaki, Manabu, Sakamoto, Shinji, Someya, Toshiyuki, Egawa, Jun, Usami, Masahide, Kodaira, Masaki, Yoshimi, Akira, Oya-Ito, Tomoko, Aleksic, Branko, Ohno, Kinji, and Ozaki, Norio

Published
2018
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17. Investigation of OLIG2 as a candidate gene for schizophrenia and autism spectrum disorder

Author

Furuta, Sho, Aleksic, Branko, Nawa, Yoshihiro, Kimura, Hiroki, Kushima, Itaru, Ishizuka, Kanako, Kato, Hidekazu, Toyama, Miho, Arioka, Yuko, Mori, Daisuke, Morikawa, Mako, Inada, Toshiya, Ozaki, Norio, Furuta, Sho, Aleksic, Branko, Nawa, Yoshihiro, Kimura, Hiroki, Kushima, Itaru, Ishizuka, Kanako, Kato, Hidekazu, Toyama, Miho, Arioka, Yuko, Mori, Daisuke, Morikawa, Mako, Inada, Toshiya, and Ozaki, Norio

Abstract

A number of genomic mutations that are thought to be strongly involved in the development of schizophrenia (SCZ) and autism spectrum disorder (ASD) have been identified. Abnormalities involving oligodendrocytes have been reported in SCZ, and as a related gene, oligodendrocyte lineage transcription factor 2 (OLIG2) has been reported to be strongly associated with SCZ. In this study, based on the common disease–rare variant hypothesis, target sequencing of candidate genes was performed to identify rare mutations with a high effect size and the possibility that the identified mutations may increase the risks of SCZ and ASD in the Japanese population. In this study, the exon region of OLIG2 was targeted; 370 patients with SCZ and 192 with ASD were subjected to next-generation sequencing. As a result, one rare missense mutation (A33T) was detected. We used the Sanger method to validate this missense mutation with a low frequency (<1%), and then carried out a genetic association analysis involving 3299 unrelated individuals (1447 with SCZ, 380 with ASD, and 1472 healthy controls) to clarify whether A33T was associated with SCZ or ASD. A33T was not found in either case group, and in only one control. We did not find evidence that p.A33T is involved in the onset of ASD or SCZ; however, associations with this variant need to be evaluated in larger samples to confirm our results., This is an Open Access article distributed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License. To view the details of this license, please visit (http://creativecommons.org/licenses/by-nc-nd/4.0/).

Published
2022

18. Cross-Disorder Analysis of Genic and Regulatory Copy Number Variations in Bipolar Disorder, Schizophrenia, and Autism Spectrum Disorder

Author

Kushima, Itaru, Nakatochi, Masahiro, Aleksic, Branko, Okada, Takashi, Kimura, Hiroki, Kato, Hidekazu, Morikawa, Mako, Inada, Toshiya, Ishizuka, Kanako, Torii, Youta, Nakamura, Yukako, Tanaka, Satoshi, Imaeda, Miho, Takahashi, Nagahide, Yamamoto, Maeri, Iwamoto, Kunihiro, Nawa, Yoshihiro, Ogawa, Nanayo, Iritani, Shuji, Hayashi, Yu, Lo, Tzuyao, Otgonbayar, Gantsooj, Furuta, Sho, Iwata, Nakao, Ikeda, Masashi, Saito, Takeo, Ninomiya, Kohei, Okochi, Tomo, Hashimoto, Ryota, Yamamori, Hidenaga, Yasuda, Yuka, Fujimoto, Michiko, Miura, Kenichiro, Itokawa, Masanari, Arai, Makoto, Miyashita, Mitsuhiro, Toriumi, Kazuya, Ohi, Kazutaka, Shioiri, Toshiki, Kitaichi, Kiyoyuki, Someya, Toshiyuki, Watanabe, Yuichiro, Egawa, Jun, Takahashi, Tsutomu, Suzuki, Michio, Sasaki, Tsukasa, Tochigi, Mamoru, Nishimura, Fumichika, Yamasue, Hidenori, Kuwabara, Hitoshi, Wakuda, Tomoyasu, Kato, Takahiro A., Kanba, Shigenobu, Horikawa, Hideki, Usami, Masahide, Kodaira, Masaki, Watanabe, Kyota, Yoshikawa, Takeo, Toyota, Tomoko, Yokoyama, Shigeru, Munesue, Toshio, Kimura, Ryo, Funabiki, Yasuko, Kosaka, Hirotaka, Jung, Minyoung, Kasai, Kiyoto, Ikegame, Tempei, Jinde, Seiichiro, Numata, Shusuke, Kinoshita, Makoto, Kato, Tadafumi, Kakiuchi, Chihiro, Yamakawa, Kazuhiro, Suzuki, Toshimitsu, Hashimoto, Naoki, Ishikawa, Shuhei, Yamagata, Bun, Nio, Shintaro, Murai, Toshiya, Son, Shuraku, Kunii, Yasuto, Yabe, Hirooki, Inagaki, Masumi, Goto, Yu-ichi, Okumura, Yuto, Ito, Tomoya, Arioka, Yuko, Mori, Daisuke, Ozaki, Norio, Kushima, Itaru, Nakatochi, Masahiro, Aleksic, Branko, Okada, Takashi, Kimura, Hiroki, Kato, Hidekazu, Morikawa, Mako, Inada, Toshiya, Ishizuka, Kanako, Torii, Youta, Nakamura, Yukako, Tanaka, Satoshi, Imaeda, Miho, Takahashi, Nagahide, Yamamoto, Maeri, Iwamoto, Kunihiro, Nawa, Yoshihiro, Ogawa, Nanayo, Iritani, Shuji, Hayashi, Yu, Lo, Tzuyao, Otgonbayar, Gantsooj, Furuta, Sho, Iwata, Nakao, Ikeda, Masashi, Saito, Takeo, Ninomiya, Kohei, Okochi, Tomo, Hashimoto, Ryota, Yamamori, Hidenaga, Yasuda, Yuka, Fujimoto, Michiko, Miura, Kenichiro, Itokawa, Masanari, Arai, Makoto, Miyashita, Mitsuhiro, Toriumi, Kazuya, Ohi, Kazutaka, Shioiri, Toshiki, Kitaichi, Kiyoyuki, Someya, Toshiyuki, Watanabe, Yuichiro, Egawa, Jun, Takahashi, Tsutomu, Suzuki, Michio, Sasaki, Tsukasa, Tochigi, Mamoru, Nishimura, Fumichika, Yamasue, Hidenori, Kuwabara, Hitoshi, Wakuda, Tomoyasu, Kato, Takahiro A., Kanba, Shigenobu, Horikawa, Hideki, Usami, Masahide, Kodaira, Masaki, Watanabe, Kyota, Yoshikawa, Takeo, Toyota, Tomoko, Yokoyama, Shigeru, Munesue, Toshio, Kimura, Ryo, Funabiki, Yasuko, Kosaka, Hirotaka, Jung, Minyoung, Kasai, Kiyoto, Ikegame, Tempei, Jinde, Seiichiro, Numata, Shusuke, Kinoshita, Makoto, Kato, Tadafumi, Kakiuchi, Chihiro, Yamakawa, Kazuhiro, Suzuki, Toshimitsu, Hashimoto, Naoki, Ishikawa, Shuhei, Yamagata, Bun, Nio, Shintaro, Murai, Toshiya, Son, Shuraku, Kunii, Yasuto, Yabe, Hirooki, Inagaki, Masumi, Goto, Yu-ichi, Okumura, Yuto, Ito, Tomoya, Arioka, Yuko, Mori, Daisuke, and Ozaki, Norio

Abstract

BACKGROUND: We aimed to determine the similarities and differences in the roles of genic and regulatory copy number variations (CNVs) in bipolar disorder (BD), schizophrenia (SCZ), and autism spectrum disorder (ASD). METHODS: Based on high-resolution CNV data from 8708 Japanese samples, we performed to our knowledge the largest cross-disorder analysis of genic and regulatory CNVs in BD, SCZ, and ASD. RESULTS: In genic CNVs, we found an increased burden of smaller (<100 kb) exonic deletions in BD, which contrasted with the highest burden of larger (>500 kb) exonic CNVs in SCZ/ASD. Pathogenic CNVs linked to neurodevelopmental disorders were significantly associated with the risk for each disorder, but BD and SCZ/ASD differed in terms of the effect size (smaller in BD) and subtype distribution of CNVs linked to neurodevelopmental disorders. We identified 3 synaptic genes (DLG2, PCDH15, and ASTN2) as risk factors for BD. Whereas gene set analysis showed that BD-associated pathways were restricted to chromatin biology, SCZ and ASD involved more extensive and similar pathways. Nevertheless, a correlation analysis of gene set results indicated weak but significant pathway similarities between BD and SCZ or ASD (r = 0.25–0.31). In SCZ and ASD, but not BD, CNVs were significantly enriched in enhancers and promoters in brain tissue. CONCLUSIONS: BD and SCZ/ASD differ in terms of CNV burden, characteristics of CNVs linked to neurodevelopmental disorders, and regulatory CNVs. On the other hand, they have shared molecular mechanisms, including chromatin biology. The BD risk genes identified here could provide insight into the pathogenesis of BD.

Published
2022

21. Additional file 1 of Functional characterization of rare NRXN1 variants identified in autism spectrum disorders and schizophrenia

Author

Ishizuka, Kanako, Yoshida, Tomoyuki, Kawabata, Takeshi, Imai, Ayako, Mori, Hisashi, Kimura, Hiroki, Inada, Toshiya, Okahisa, Yuko, Egawa, Jun, Usami, Masahide, Itaru Kushima, Morikawa, Mako, Okada, Takashi, Ikeda, Masashi, Aleksic Branko, Mori, Daisuke, Someya, Toshiyuki, Nakao Iwata, and Ozaki, Norio

Abstract

Additional file 1 Supplementary Figures and Tables. Figure S1. Family-trio analysis with parental genotype data. Figure S2. Decreased NLGN1 binding activities of T737M and D772G variants. Figure S3. A modeled 3D complex structure of NLGN1 with NRXN1a. Figure S4. Six chosen model structures of LNS4 domain with the complex-type N-glycan among the 300 generated conformations. Figure S5. A schematic view of the complex-type N-glycan taken from PDB entry 4fqc. Figure S6. Locations of the LNS4 missense mutations in NRXN1a (PDB ID:3r05) with a modeled loop with N-glycan. Table S1. Overview of eight control SNVs in NRXN1-LNS4. Table S2. Overview of SNVs for in vitro functional assay and 3D models of structures. Table S3. Cross tabulation of variants for cell surface expression and N-glycan model. Table S4. Cross tabulation of variants for interaction with NLGN1 and stability change.

Published
2020
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23. Validation and factor structure of the Japanese version of the inventory to diagnose depression, lifetime version for pregnant women

Author

Kubota, Chika, primary, Inada, Toshiya, additional, Nakamura, Yukako, additional, Shiino, Tomoko, additional, Ando, Masahiko, additional, Aleksic, Branko, additional, Yamauchi, Aya, additional, Morikawa, Mako, additional, Okada, Takashi, additional, Ohara, Masako, additional, Sato, Maya, additional, Murase, Satomi, additional, Goto, Setsuko, additional, Kanai, Atsuko, additional, and Ozaki, Norio, additional

Published
2020
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24. The Risk Factors Predicting Suicidal Ideation Among Perinatal Women in Japan

Author

Kubota, Chika, primary, Inada, Toshiya, additional, Shiino, Tomoko, additional, Ando, Masahiko, additional, Sato, Maya, additional, Nakamura, Yukako, additional, Yamauchi, Aya, additional, Morikawa, Mako, additional, Okada, Takashi, additional, Ohara, Masako, additional, Aleksic, Branko, additional, Murase, Satomi, additional, Goto, Setsuko, additional, Kanai, Atsuko, additional, and Ozaki, Norio, additional

Published
2020
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25. Additional file 1: of Methylation analysis for postpartum depression: a case control study

Author

Nakamura, Yukako, Nakatochi, Masahiro, Shohko Kunimoto, Okada, Takashi, Aleksic, Branko, Toyama, Miho, Shiino, Tomoko, Morikawa, Mako, Yamauchi, Aya, Yoshimi, Akira, Furukawa-Hibi, Yoko, Nagai, Taku, Ohara, Masako, Kubota, Chika, Kiyofumi Yamada, Ando, Masahiko, and Ozaki, Norio

Subjects
body regions, nervous system, fungi, behavioral disciplines and activities
Abstract

Questionnaire. It shows items of the self-reporting questionnaire we used in this study. (PDF 83 kb)

Published
2019
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26. Relation Between Perinatal Depressive Symptoms, Harm Avoidance, and a History of Major Depressive Disorder: A Cohort Study of Pregnant Women in Japan

Author

Kubota, Chika, primary, Inada, Toshiya, additional, Shiino, Tomoko, additional, Ando, Masahiko, additional, Aleksic, Branko, additional, Yamauchi, Aya, additional, Sato, Maya, additional, Ohara, Masako, additional, Murase, Satomi, additional, Morikawa, Mako, additional, Nakamura, Yukako, additional, Okada, Takashi, additional, Goto, Setsuko, additional, Kanai, Atsuko, additional, and Ozaki, Norio, additional

Published
2019
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28. Comparative Analyses of Copy-Number Variation in Autism Spectrum Disorder and Schizophrenia Reveal Etiological Overlap and Biological Insights

Author

Kushima, Itaru, primary, Aleksic, Branko, additional, Nakatochi, Masahiro, additional, Shimamura, Teppei, additional, Okada, Takashi, additional, Uno, Yota, additional, Morikawa, Mako, additional, Ishizuka, Kanako, additional, Shiino, Tomoko, additional, Kimura, Hiroki, additional, Arioka, Yuko, additional, Yoshimi, Akira, additional, Takasaki, Yuto, additional, Yu, Yanjie, additional, Nakamura, Yukako, additional, Yamamoto, Maeri, additional, Iidaka, Tetsuya, additional, Iritani, Shuji, additional, Inada, Toshiya, additional, Ogawa, Nanayo, additional, Shishido, Emiko, additional, Torii, Youta, additional, Kawano, Naoko, additional, Omura, Yutaka, additional, Yoshikawa, Toru, additional, Uchiyama, Tokio, additional, Yamamoto, Toshimichi, additional, Ikeda, Masashi, additional, Hashimoto, Ryota, additional, Yamamori, Hidenaga, additional, Yasuda, Yuka, additional, Someya, Toshiyuki, additional, Watanabe, Yuichiro, additional, Egawa, Jun, additional, Nunokawa, Ayako, additional, Itokawa, Masanari, additional, Arai, Makoto, additional, Miyashita, Mitsuhiro, additional, Kobori, Akiko, additional, Suzuki, Michio, additional, Takahashi, Tsutomu, additional, Usami, Masahide, additional, Kodaira, Masaki, additional, Watanabe, Kyota, additional, Sasaki, Tsukasa, additional, Kuwabara, Hitoshi, additional, Tochigi, Mamoru, additional, Nishimura, Fumichika, additional, Yamasue, Hidenori, additional, Eriguchi, Yosuke, additional, Benner, Seico, additional, Kojima, Masaki, additional, Yassin, Walid, additional, Munesue, Toshio, additional, Yokoyama, Shigeru, additional, Kimura, Ryo, additional, Funabiki, Yasuko, additional, Kosaka, Hirotaka, additional, Ishitobi, Makoto, additional, Ohmori, Tetsuro, additional, Numata, Shusuke, additional, Yoshikawa, Takeo, additional, Toyota, Tomoko, additional, Yamakawa, Kazuhiro, additional, Suzuki, Toshimitsu, additional, Inoue, Yushi, additional, Nakaoka, Kentaro, additional, Goto, Yu-ichi, additional, Inagaki, Masumi, additional, Hashimoto, Naoki, additional, Kusumi, Ichiro, additional, Son, Shuraku, additional, Murai, Toshiya, additional, Ikegame, Tempei, additional, Okada, Naohiro, additional, Kasai, Kiyoto, additional, Kunimoto, Shohko, additional, Mori, Daisuke, additional, Iwata, Nakao, additional, and Ozaki, Norio, additional

Published
2018
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30. Possible involvement of a cell adhesion molecule, Migfilin, in brain development and pathogenesis of autism spectrum disorders

Author

Ishizuka, Kanako, primary, Tabata, Hidenori, additional, Ito, Hidenori, additional, Kushima, Itaru, additional, Noda, Mariko, additional, Yoshimi, Akira, additional, Usami, Masahide, additional, Watanabe, Kyota, additional, Morikawa, Mako, additional, Uno, Yota, additional, Okada, Takashi, additional, Mori, Daisuke, additional, Aleksic, Branko, additional, Ozaki, Norio, additional, and Nagata, Koh-ichi, additional

Published
2017
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31. Social support helps protect against perinatal bonding failure and depression among mothers: a prospective cohort study

Author

Ohara, Masako, primary, Okada, Takashi, additional, Aleksic, Branko, additional, Morikawa, Mako, additional, Kubota, Chika, additional, Nakamura, Yukako, additional, Shiino, Tomoko, additional, Yamauchi, Aya, additional, Uno, Yota, additional, Murase, Satomi, additional, Goto, Setsuko, additional, Kanai, Atsuko, additional, Masuda, Tomoko, additional, Nakatochi, Masahiro, additional, Ando, Masahiko, additional, and Ozaki, Norio, additional

Published
2017
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34. Validation and factor analysis of mother-infant bonding questionnaire in pregnant and postpartum women in Japan

Author

Ohara, Masako, primary, Okada, Takashi, additional, Kubota, Chika, additional, Nakamura, Yukako, additional, Shiino, Tomoko, additional, Aleksic, Branko, additional, Morikawa, Mako, additional, Yamauchi, Aya, additional, Uno, Yota, additional, Murase, Satomi, additional, Goto, Setsuko, additional, Kanai, Atsuko, additional, Masuda, Tomoko, additional, and Ozaki, Norio, additional

Published
2016
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37. Relationship between social support during pregnancy and postpartum depressive state: a prospective cohort study

Author

Morikawa, Mako, primary, Okada, Takashi, additional, Ando, Masahiko, additional, Aleksic, Branko, additional, Kunimoto, Shohko, additional, Nakamura, Yukako, additional, Kubota, Chika, additional, Uno, Yota, additional, Tamaji, Ai, additional, Hayakawa, Norika, additional, Furumura, Kaori, additional, Shiino, Tomoko, additional, Morita, Tokiko, additional, Ishikawa, Naoko, additional, Ohoka, Harue, additional, Usui, Hinako, additional, Banno, Naomi, additional, Murase, Satomi, additional, Goto, Setsuko, additional, Kanai, Atsuko, additional, Masuda, Tomoko, additional, and Ozaki, Norio, additional

Published
2015
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38. Factor Structure of the Japanese Version of the Edinburgh Postnatal Depression Scale in the Postpartum Period

Author

Kubota, Chika, primary, Okada, Takashi, additional, Aleksic, Branko, additional, Nakamura, Yukako, additional, Kunimoto, Shohko, additional, Morikawa, Mako, additional, Shiino, Tomoko, additional, Tamaji, Ai, additional, Ohoka, Harue, additional, Banno, Naomi, additional, Morita, Tokiko, additional, Murase, Satomi, additional, Goto, Setsuko, additional, Kanai, Atsuko, additional, Masuda, Tomoko, additional, Ando, Masahiko, additional, and Ozaki, Norio, additional

Published
2014
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39. Integrative Analyses of De NovoMutations Provide Deeper Biological Insights into Autism Spectrum Disorder

Author

Takata, Atsushi, Miyake, Noriko, Tsurusaki, Yoshinori, Fukai, Ryoko, Miyatake, Satoko, Koshimizu, Eriko, Kushima, Itaru, Okada, Takashi, Morikawa, Mako, Uno, Yota, Ishizuka, Kanako, Nakamura, Kazuhiko, Tsujii, Masatsugu, Yoshikawa, Takeo, Toyota, Tomoko, Okamoto, Nobuhiko, Hiraki, Yoko, Hashimoto, Ryota, Yasuda, Yuka, Saitoh, Shinji, Ohashi, Kei, Sakai, Yasunari, Ohga, Shouichi, Hara, Toshiro, Kato, Mitsuhiro, Nakamura, Kazuyuki, Ito, Aiko, Seiwa, Chizuru, Shirahata, Emi, Osaka, Hitoshi, Matsumoto, Ayumi, Takeshita, Saoko, Tohyama, Jun, Saikusa, Tomoko, Matsuishi, Toyojiro, Nakamura, Takumi, Tsuboi, Takashi, Kato, Tadafumi, Suzuki, Toshifumi, Saitsu, Hirotomo, Nakashima, Mitsuko, Mizuguchi, Takeshi, Tanaka, Fumiaki, Mori, Norio, Ozaki, Norio, and Matsumoto, Naomichi

Abstract

Recent studies have established important roles of de novomutations (DNMs) in autism spectrum disorders (ASDs). Here, we analyze DNMs in 262 ASD probands of Japanese origin and confirm the “de novoparadigm” of ASDs across ethnicities. Based on this consistency, we combine the lists of damaging DNMs in our and published ASD cohorts (total number of trios, 4,244) and perform integrative bioinformatics analyses. Besides replicating the findings of previous studies, our analyses highlight ATP-binding genes and fetal cerebellar/striatal circuits. Analysis of individual genes identified 61 genes enriched for damaging DNMs, including ten genes for which our dataset now contributes to statistical significance. Screening of compounds altering the expression of genes hit by damaging DNMs reveals a global downregulating effect of valproic acid, a known risk factor for ASDs, whereas cardiac glycosides upregulate these genes. Collectively, our integrative approach provides deeper biological and potential medical insights into ASDs.

Published
2018
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41. In vitro susceptibility testing of phytochemicals from essential oils against Prototheca species.

Author

Nojo H, Ishijima SA, Morikawa M, Ito T, and Kano R

Subjects
Animals, Cattle, Monoterpenes pharmacology, Female, Mastitis, Bovine microbiology, Mastitis, Bovine drug therapy, Oils, Volatile pharmacology, Thymol pharmacology, Prototheca drug effects, Microbial Sensitivity Tests, Cymenes pharmacology, Phytochemicals pharmacology, Acyclic Monoterpenes pharmacology
Abstract

Phytochemicals isolated from essential oils are effective alternatives for inhibiting microbial pathogens. Bovine protothecal mastitis is the cause of a reduction in milk production and the secretion of thin, watery milk with white flakes. In the present study, we performed in vitro susceptibility testing of the phytochemicals carvacrol, citral, and thymol in Prototheca strains isolated from cases of protothecosis in small animals and cow feces. The susceptibility of the algae to carvacrol, citral, and thymol was assessed using the modified CLSI M27-A3 broth microdilution method. The ranges of the minimum inhibitory concentrations (MIC%) of the phytochemicals in all isolates were 0.03% to 0.125% for carvacrol, 0.03% to 0.25% for citral, and 0.06% to 0.25% for thymol. Based on these results, carvacrol, citral, and thymol appear effective against Prototheca species at the tested concentrations, and may thus be useful for environmental disinfection in barns.

Published
2024
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42. Investigation of OLIG2 as a candidate gene for schizophrenia and autism spectrum disorder.

Author

Furuta S, Aleksic B, Nawa Y, Kimura H, Kushima I, Ishizuka K, Kato H, Toyama M, Arioka Y, Mori D, Morikawa M, Inada T, and Ozaki N

Subjects
Humans, Mutation, Mutation, Missense genetics, Autism Spectrum Disorder genetics, Oligodendrocyte Transcription Factor 2 genetics, Schizophrenia genetics
Abstract

A number of genomic mutations that are thought to be strongly involved in the development of schizophrenia (SCZ) and autism spectrum disorder (ASD) have been identified. Abnormalities involving oligodendrocytes have been reported in SCZ, and as a related gene, oligodendrocyte lineage transcription factor 2 ( OLIG2 ) has been reported to be strongly associated with SCZ. In this study, based on the common disease-rare variant hypothesis, target sequencing of candidate genes was performed to identify rare mutations with a high effect size and the possibility that the identified mutations may increase the risks of SCZ and ASD in the Japanese population. In this study, the exon region of OLIG2 was targeted; 370 patients with SCZ and 192 with ASD were subjected to next-generation sequencing. As a result, one rare missense mutation (A33T) was detected. We used the Sanger method to validate this missense mutation with a low frequency (<1%), and then carried out a genetic association analysis involving 3299 unrelated individuals (1447 with SCZ, 380 with ASD, and 1472 healthy controls) to clarify whether A33T was associated with SCZ or ASD. A33T was not found in either case group, and in only one control. We did not find evidence that p.A33T is involved in the onset of ASD or SCZ; however, associations with this variant need to be evaluated in larger samples to confirm our results., Competing Interests: All authors have no conflicts of interest to declare.

Published
2022
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43. Integrative Analyses of De Novo Mutations Provide Deeper Biological Insights into Autism Spectrum Disorder.

Author

Takata A, Miyake N, Tsurusaki Y, Fukai R, Miyatake S, Koshimizu E, Kushima I, Okada T, Morikawa M, Uno Y, Ishizuka K, Nakamura K, Tsujii M, Yoshikawa T, Toyota T, Okamoto N, Hiraki Y, Hashimoto R, Yasuda Y, Saitoh S, Ohashi K, Sakai Y, Ohga S, Hara T, Kato M, Nakamura K, Ito A, Seiwa C, Shirahata E, Osaka H, Matsumoto A, Takeshita S, Tohyama J, Saikusa T, Matsuishi T, Nakamura T, Tsuboi T, Kato T, Suzuki T, Saitsu H, Nakashima M, Mizuguchi T, Tanaka F, Mori N, Ozaki N, and Matsumoto N

Subjects
Autism Spectrum Disorder pathology, Genetic Predisposition to Disease, Humans, Autism Spectrum Disorder genetics, Mutation genetics
Abstract

Recent studies have established important roles of de novo mutations (DNMs) in autism spectrum disorders (ASDs). Here, we analyze DNMs in 262 ASD probands of Japanese origin and confirm the "de novo paradigm" of ASDs across ethnicities. Based on this consistency, we combine the lists of damaging DNMs in our and published ASD cohorts (total number of trios, 4,244) and perform integrative bioinformatics analyses. Besides replicating the findings of previous studies, our analyses highlight ATP-binding genes and fetal cerebellar/striatal circuits. Analysis of individual genes identified 61 genes enriched for damaging DNMs, including ten genes for which our dataset now contributes to statistical significance. Screening of compounds altering the expression of genes hit by damaging DNMs reveals a global downregulating effect of valproic acid, a known risk factor for ASDs, whereas cardiac glycosides upregulate these genes. Collectively, our integrative approach provides deeper biological and potential medical insights into ASDs., (Copyright © 2018 The Authors. Published by Elsevier Inc. All rights reserved.)

Published
2018
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