Updated on 2021/11/16

写真a

 
DAISUKE Mori
 
Organization
Brain and Mind Research Center Division Designated associate professor
Title
Designated associate professor

Degree 1

  1. 博士(理学) ( 2003.3   東北大学 ) 

Research Interests 10

  1. 脳・神経

  2. 統合失調症

  3. 細胞内輸送

  4. 神経細胞

  5. developmental disorder

  6. 極性

  7. 包括脳ネットワーク

  8. プロテオーム

  9. シグナル伝達

  10. ゴルジ体

Research Areas 2

  1. Life Science / Medical biochemistry  / Psychiatry

  2. Life Science / Molecular biology

Research History 1

  1. Nagoya University   Brain and Mind Research Center   Designated associate professor

    2016.6

Education 2

  1. Tohoku University   Science   Chemistry

  2. Tohoku University   Science   Chemistry, Doctor course

Professional Memberships 2

  1. The Japan Neuroscience Society

  2. The Molecular Biology Society of Japan

 

Papers 14

  1. ARHGAP10, which encodes Rho GTPase-activating protein 10, is a novel gene for schizophrenia risk Reviewed

    Mariko Sekiguchi, Akira Sobue, Itaru Kushima, Chenyao Wang, Yuko Arioka, Hidekazu Kato, Akiko Kodama, Hisako Kubo, Norimichi Ito, Masahito Sawahata, Kazuhiro Hada, Ryosuke Ikeda, Mio Shinno, Chikara Mizukoshi, Keita Tsujimura, Akira Yoshimi, Kanako Ishizuka, Yuto Takasaki, Hiroki Kimura, Jingrui Xing, Yanjie Yu, Maeri Yamamoto, Takashi Okada, Emiko Shishido, Toshiya Inada, Masahiro Nakatochi, Tetsuya Takano, Keisuke Kuroda, Mutsuki Amano, Branko Aleksic, Takashi Yamomoto, Tetsushi Sakuma, Tomomi Aida, Kohichi Tanaka, Ryota Hashimoto, Makoto Arai, Masashi Ikeda, Nakao Iwata, Teppei Shimamura, Taku Nagai, Toshitaka Nabeshima, Kozo Kaibuchi, Kiyofumi Yamada, Daisuke Mori, Norio Ozaki

    Translational Psychiatry   Vol. 10 ( 1 )   2020.12

     More details

    Authorship:Corresponding author   Language:English   Publishing type:Research paper (scientific journal)   Publisher:Springer Science and Business Media LLC  

    DOI: 10.1038/s41398-020-00917-z

    Other Link: http://www.nature.com/articles/s41398-020-00917-z

  2. Generation and analysis of novel Reln-deleted mouse model corresponding to exonic Reln deletion in schizophrenia. Reviewed International journal

    Masahito Sawahata, Daisuke Mori, Yuko Arioka, Hisako Kubo, Itaru Kushima, Kanako Kitagawa, Akira Sobue, Emiko Shishido, Mariko Sekiguchi, Akiko Kodama, Ryosuke Ikeda, Branko Aleksic, Hiroki Kimura, Kanako Ishizuka, Taku Nagai, Kozo Kaibuchi, Toshitaka Nabeshima, Kiyofumi Yamada, Norio Ozaki

    Psychiatry and clinical neurosciences     2020.2

     More details

    Authorship:Corresponding author   Language:English   Publishing type:Research paper (scientific journal)  

    AIMS: A Japanese individual with schizophrenia harboring a novel exonic deletion in RELN was recently identified by genome-wide copy-number variation analysis. Thus, the present study aimed to generate and analyze a model mouse to clarify whether RELN deficiency is associated with the pathogenesis of schizophrenia. METHODS: A mouse line with a novel RELN exonic deletion (Reln-del) was established using the CRISPR/Cas9 method to elucidate the underlying molecular mechanism. Subsequently, general behavioral tests and histopathological examinations of the model mice were conducted and phenotypic analysis of the cerebellar granule cell migration was performed. RESULTS: The phenotype of homozygous Reln-del mice was similar to that of reeler mice with cerebellar atrophy, dysplasia of the cerebral layers, and abrogated protein levels of cerebral reelin. The expression of reelin in heterozygous Reln-del mice was approximately half of that in wild-type mice. Conversely, behavioral analyses in heterozygous Reln-del mice without cerebellar atrophy or dysplasia showed abnormal social novelty in the three-chamber social interaction test. In vitro reaggregation formation and neuronal migration were severely altered in the cerebellar cultures of homozygous Reln-del mice. CONCLUSIONS: The present results in novel Reln-del mice modeled after our patient with a novel exonic deletion in RELN are expected to contribute to the development of reelin-based therapies for schizophrenia. This article is protected by copyright. All rights reserved.

    DOI: 10.1111/pcn.12993

    PubMed

  3. Comprehensive analysis of a novel mouse model of the 22q11.2 deletion syndrome: a model with the most common 3.0-Mb deletion at the human 22q11.2 locus. Reviewed International journal

    Ryo Saito, Michinori Koebis, Taku Nagai, Kimiko Shimizu, Jingzhu Liao, Bolati Wulaer, Yuki Sugaya, Kenichiro Nagahama, Naofumi Uesaka, Itaru Kushima, Daisuke Mori, Kazuaki Maruyama, Kazuki Nakao, Hiroki Kurihara, Kiyofumi Yamada, Masanobu Kano, Yoshitaka Fukada, Norio Ozaki, Atsu Aiba

    Translational psychiatry   Vol. 10 ( 1 ) page: 35 - 35   2020.2

     More details

    Language:English   Publishing type:Research paper (scientific journal)  

    The 22q11.2 deletion syndrome (22q11.2DS) is associated with an increased risk for psychiatric disorders. Although most of the 22q11.2DS patients have a 3.0-Mb deletion, existing mouse models only mimic a minor mutation of 22q11.2DS, a 1.5-Mb deletion. The role of the genes existing outside the 1.5-Mb deletion in psychiatric symptoms of 22q11.2DS is unclear. In this study, we generated a mouse model that reproduced the 3.0-Mb deletion of the 22q11.2DS (Del(3.0 Mb)/ +) using the CRISPR/Cas9 system. Ethological and physiological phenotypes of adult male mutants were comprehensively evaluated by visual-evoked potentials, circadian behavioral rhythm, and a series of behavioral tests, such as measurement of locomotor activity, prepulse inhibition, fear-conditioning memory, and visual discrimination learning. As a result, Del(3.0 Mb)/ + mice showed reduction of auditory prepulse inhibition and attenuated cue-dependent fear memory, which is consistent with the phenotypes of existing 22q11.2DS models. In addition, Del(3.0 Mb)/ + mice displayed an impaired early visual processing that is commonly seen in patients with schizophrenia. Meanwhile, unlike the existing models, Del(3.0 Mb)/ + mice exhibited hypoactivity over several behavioral tests, possibly reflecting the fatigability of 22q11.2DS patients. Lastly, Del(3.0 Mb)/ + mice displayed a faster adaptation to experimental jet lag as compared with wild-type mice. Our results support the validity of Del(3.0 Mb)/ + mice as a schizophrenia animal model and suggest that our mouse model is a useful resource to understand pathogenic mechanisms of schizophrenia and other psychiatric disorders associated with 22q11.2DS.

    DOI: 10.1038/s41398-020-0723-z

    PubMed

  4. Characterization of a schizophrenia patient with a rare RELN deletion by combining genomic and patient-derived cell analyses. Reviewed International journal

    Yuko Arioka, Akihiro Hirata, Itaru Kushima, Branko Aleksic, Daisuke Mori, Norio Ozaki

    Schizophrenia research     2019.12

     More details

    Language:English  

    Genetic studies have identified rare RELN variants as risk factors for psychiatric disorders. However, additional genetic factors appear to be necessary for disease onset. Detailed genetic information and the use of patient-derived neuronal cells may thus enable to discover these disease-related additional factors. Here, we performed whole-genome sequencing of a schizophrenia patient with a rare RELN deletion and his healthy mother, and examined the phenotypes of 3D-cultured neuronal cells derived from induced pluripotent stem cells of this patient. Our results revealed that, along with the RELN deletion, neuronal death was promoted in this patient; thus, neuronal death may be a vulnerable factor for schizophrenia.

    DOI: 10.1016/j.schres.2019.10.038

    PubMed

  5. In Vitro Modeling of the Bipolar Disorder and Schizophrenia Using Patient-Derived Induced Pluripotent Stem Cells with Copy Number Variations of PCDH15 and RELN Reviewed

    Takaya Ishii, Mitsuru Ishikawa, Koki Fujimori, Takuji Maeda, Itaru Kushima, Yuko Arioka, Daisuke Mori, Yuhki Nakatake, Bun Yamagata, Shintaro Nio, Takahiro A. Kato, Nan Yang, Marius Wernig, Shigenobu Kanba, Masaru Mimura, Norio Ozaki, Hideyuki Okano

    eneuro     page: ENEURO.0403   2019.9

     More details

    Publisher:Society for Neuroscience  

    DOI: 10.1523/ENEURO.0403-18.2019

  6. Reorganization of brain networks and its association with general cognitive performance over the adult lifespan. Reviewed International journal

    Epifanio Bagarinao, Hirohisa Watanabe, Satoshi Maesawa, Daisuke Mori, Kazuhiro Hara, Kazuya Kawabata, Noritaka Yoneyama, Reiko Ohdake, Kazunori Imai, Michihito Masuda, Takamasa Yokoi, Aya Ogura, Toshiaki Taoka, Shuji Koyama, Hiroki C Tanabe, Masahisa Katsuno, Toshihiko Wakabayashi, Masafumi Kuzuya, Norio Ozaki, Minoru Hoshiyama, Haruo Isoda, Shinji Naganawa, Gen Sobue

    Scientific reports   Vol. 9 ( 1 ) page: 11352 - 11352   2019.8

     More details

    Language:English   Publisher:Springer Science and Business Media {LLC}  

    Healthy aging is associated with structural and functional changes in the brain even in individuals who are free of neurodegenerative diseases. Using resting state functional magnetic resonance imaging data from a carefully selected cohort of participants, we examined cross sectional changes in the functional organization of several large-scale brain networks over the adult lifespan and its potential association with general cognitive performance. Converging results from multiple analyses at the voxel, node, and network levels showed widespread reorganization of functional brain networks with increasing age. Specifically, the primary processing (visual and sensorimotor) and visuospatial (dorsal attention) networks showed diminished network integrity, while the so-called core neurocognitive (executive control, salience, and default mode) and basal ganglia networks exhibited relatively preserved between-network connections. The visuospatial and precuneus networks also showed significantly more widespread increased connectivity with other networks. Graph analysis suggested that this reorganization progressed towards a more integrated network topology. General cognitive performance, assessed by Addenbrooke's Cognitive Examination-Revised total score, was positively correlated with between-network connectivity among the core neurocognitive and basal ganglia networks and the integrity of the primary processing and visuospatial networks. Mediation analyses further indicated that the observed association between aging and relative decline in cognitive performance could be mediated by changes in relevant functional connectivity measures. Overall, these findings provided further evidence supporting widespread age-related brain network reorganization and its potential association with general cognitive performance during healthy aging.

    DOI: 10.1038/s41598-019-47922-x

    PubMed

  7. Quantitative facial expression analysis revealed the efficacy and time course of oxytocin in autism.

    Owada K, Okada T, Munesue T, Kuroda M, Fujioka T, Uno Y, Matsumoto K, Kuwabara H, Mori D, Okamoto Y, Yoshimura Y, Kawakubo Y, Arioka Y, Kojima M, Yuhi T, Yassin W, Kushima I, Benner S, Ogawa N, Kawano N, Eriguchi Y, Uemura Y, Yamamoto M, Kano Y, Kasai K, Higashida H, Ozaki N, Kosaka H, Yamasue H

    Brain : a journal of neurology     2019.5

     More details

    Language:English   Publishing type:Research paper (scientific journal)  

    DOI: 10.1093/brain/awz126

    PubMed

  8. Author Correction: Proteomic analysis of lymphoblastoid cell lines from schizophrenic patients. Reviewed International journal

    Akira Yoshimi, Shinnosuke Yamada, Shohko Kunimoto, Branko Aleksic, Akihiro Hirakawa, Mitsuki Ohashi, Yurie Matsumoto, Kazuhiro Hada, Norimichi Itoh, Yuko Arioka, Hiroki Kimura, Itaru Kushima, Yukako Nakamura, Tomoko Shiino, Daisuke Mori, Satoshi Tanaka, Shuko Hamada, Yukihiro Noda, Taku Nagai, Kiyofumi Yamada, Norio Ozaki

    Translational psychiatry   Vol. 9 ( 1 ) page: 146 - 146   2019.5

     More details

    Language:English  

    The original Article required a few updates; one co-author name, which was given as Hiroki Kiumura, has been updated to Hiroki Kimura. Furthermore, supplementary information has been updated, and grant numbers have been added. These updates have been made to both the PDF and HTML versions of this Article.

    DOI: 10.1038/s41398-019-0479-5

    PubMed

  9. Assessment of a glyoxalase I frameshift variant, p.P122fs, in Japanese patients with schizophrenia. Reviewed International journal

    Kanako Ishizuka, Hiroki Kimura, Itaru Kushima, Toshiya Inada, Yuko Okahisa, Masashi Ikeda, Nakao Iwata, Daisuke Mori, Branko Aleksic, Norio Ozaki

    Psychiatric genetics   Vol. 28 ( 5 ) page: 90 - 93   2018.10

     More details

    Language:English  

    Enhanced carbonyl stress has been observed in a subgroup of patients with schizophrenia. Glyoxalase I, which is encoded by GLO1, is an enzyme that protects against carbonyl stress. In this study, we focused on the association between rare genetic variants of GLO1 and schizophrenia. First, we identified one heterozygous frameshift variant, p.P122fs, in 370 Japanese schizophrenia cases with allele frequencies of up to 1% by exon-targeted mutation screening of GLO1. We then performed an association analysis on 1282 cases and 1764 controls with this variant. The variant was found in three cases and eight controls. There was no statistically significant association between p.P122fs in GLO1 and schizophrenia (P=0.25). This frameshift variant in GLO1 might occur at near-polymorphic frequencies in the Japanese population, although further investigations using larger samples and biological analyses are needed to exclude the possibility of a low-penetrance genetic risk associated with this variant.

    DOI: 10.1097/YPG.0000000000000204

    PubMed

  10. Comparative Analyses of Copy-Number Variation in Autism Spectrum Disorder and Schizophrenia Reveal Etiological Overlap and Biological Insights. Reviewed International journal

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

    Cell reports   Vol. 24 ( 11 ) page: 2838 - 2856   2018.9

     More details

    Language:English  

    Compelling evidence in Caucasian populations suggests a role for copy-number variations (CNVs) in autism spectrum disorder (ASD) and schizophrenia (SCZ). We analyzed 1,108 ASD cases, 2,458 SCZ cases, and 2,095 controls in a Japanese population and confirmed an increased burden of rare exonic CNVs in both disorders. Clinically significant (or pathogenic) CNVs, including those at 29 loci common to both disorders, were found in about 8% of ASD and SCZ cases, which was significantly higher than in controls. Phenotypic analysis revealed an association between clinically significant CNVs and intellectual disability. Gene set analysis showed significant overlap of biological pathways in both disorders including oxidative stress response, lipid metabolism/modification, and genomic integrity. Finally, based on bioinformatics analysis, we identified multiple disease-relevant genes in eight well-known ASD/SCZ-associated CNV loci (e.g., 22q11.2, 3q29). Our findings suggest an etiological overlap of ASD and SCZ and provide biological insights into these disorders.

    DOI: 10.1016/j.celrep.2018.08.022

    PubMed

  11. Genetic and animal model analyses reveal the pathogenic role of a novel deletion of RELN in schizophrenia Reviewed

    Sobue Akira, Kushima Itaru, Nagai Taku, Shan Wei, Kohno Takao, Aleksic Branko, Aoyama Yuki, Mori Daisuke, Arioka Yuko, Kawano Naoko

    Scientific reports   Vol. 8 ( 1 ) page: 13046   2018

  12. Three lines of induced pluripotent stem cells derived from a 15q11. 2-q13. 1 duplication syndrome patient Reviewed

    Arioka Yuko, Kushima Itaru, Mori Daisuke, Ozaki Norio

    Stem Cell Research     2018

  13. Rare genetic variants in CX3CR1 and their contribution to the increased risk of schizophrenia and autism spectrum disorders Reviewed

    K. Ishizuka, Y. Fujita, T. Kawabata, H. Kimura, Y. Iwayama, T. Inada, Y. Okahisa, J. Egawa, M. Usami, I. Kushima, Y. Uno, T. Okada, M. Ikeda, B. Aleksic, D. Mori, To Someya, T. Yoshikawa, N. Iwata, H. Nakamura, T. Yamashita, N. Ozaki

    TRANSLATIONAL PSYCHIATRY   Vol. 7 ( 8 ) page: e1184   2017.8

     More details

    Language:English   Publishing type:Research paper (scientific journal)   Publisher:NATURE PUBLISHING GROUP  

    CX3CR1, a G protein-coupled receptor solely expressed by microglia in the brain, has been repeatedly reported to be associated with neurodevelopmental disorders including schizophrenia (SCZ) and autism spectrum disorders (ASD) in transcriptomic and animal studies but not in genetic studies. To address the impacts of variants in CX3CR1 on neurodevelopmental disorders, we conducted coding exon-targeted resequencing of CX3CR1 in 370 Japanese SCZ and 192 ASD patients using next-generation sequencing technology, followed by a genetic association study in a sample comprising 7054 unrelated individuals (2653 SCZ, 574 ASD and 3827 controls). We then performed in silico three-dimensional (3D) structural modeling and in vivo disruption of Akt phosphorylation to determine the impact of the detected variant on CX3CR1-dependent signal transduction. We detected a statistically significant association between the variant Ala55Thr in CX3CR1 with SCZ and ASD phenotypes (odds ratio = 8.3, P = 0.020). A 3D structural model indicated that Ala55Thr could destabilize the conformation of the CX3CR1 helix 8 and affect its interaction with a heterotrimeric G protein. In vitro functional analysis showed that the CX3CR1-Ala55Thr mutation inhibited cell signaling induced by fractalkine, the ligand for CX3CR1. The combined data suggested that the variant Ala55Thr in CX3CR1 might result in the disruption of CX3CR1 signaling. Our results strengthen the association between microglia-specific genes and neurodevelopmental disorders.

    DOI: 10.1038/tp.2017.173

    Web of Science

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

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

    MOLECULAR PSYCHIATRY   Vol. 22 ( 3 ) page: 430 - 440   2017.3

     More details

    Language:English   Publishing type:Research paper (scientific journal)   Publisher:NATURE PUBLISHING GROUP  

    Recent schizophrenia (SCZ) studies have reported an increased burden of de novo copy number variants (CNVs) and identified specific high-risk CNVs, although with variable phenotype expressivity. However, the pathogenesis of SCZ has not been fully elucidated. Using array comparative genomic hybridization, we performed a high-resolution genome-wide CNV analysis on a mainly (92%) Japanese population (1699 SCZ cases and 824 controls) and identified 7066 rare CNVs, 70.0% of which were small (< 100 kb). Clinically significant CNVs were significantly more frequent in cases than in controls (odds ratio = 3.04, P = 9.3 x 10 (-9), 9.0% of cases). We confirmed a significant association of X-chromosome aneuploidies with SCZ and identified 11 de novo CNVs (e. g., MBD5 deletion) in cases. In patients with clinically significant CNVs, 41.7% had a history of congenital/developmental phenotypes, and the rate of treatment resistance was significantly higher (odds ratio = 2.79, P = 0.0036). We found more severe clinical manifestations in patients with two clinically significant CNVs. Gene set analysis replicated previous findings (e. g., synapse, calcium signaling) and identified novel biological pathways including oxidative stress response, genomic integrity, kinase and small GTPase signaling. Furthermore, involvement of multiple SCZ candidate genes and biological pathways in the pathogenesis of SCZ was suggested in established SCZ-associated CNV loci. Our study shows the high genetic heterogeneity of SCZ and its clinical features and raises the possibility that genomic instability is involved in its pathogenesis, which may be related to the increased burden of de novo CNVs and variable expressivity of CNVs.

    DOI: 10.1038/mp.2016.88

    Web of Science

    Other Link: http://orcid.org/0000-0002-9072-2546

▼display all

MISC 8

  1. Changes in white matter fiber density and morphology across the adult lifespan: A cross-sectional fixel-based analysis. International journal

    Shao Wei Choy, Epifanio Bagarinao, Hirohisa Watanabe, Eric Tatt Wei Ho, Satoshi Maesawa, Daisuke Mori, Kazuhiro Hara, Kazuya Kawabata, Noritaka Yoneyama, Reiko Ohdake, Kazunori Imai, Michihito Masuda, Takamasa Yokoi, Aya Ogura, Toshiaki Taoka, Shuji Koyama, Hiroki C Tanabe, Masahisa Katsuno, Toshihiko Wakabayashi, Masafumi Kuzuya, Minoru Hoshiyama, Haruo Isoda, Shinji Naganawa, Norio Ozaki, Gen Sobue

    Human brain mapping     2020.4

     More details

    Language:English  

    White matter (WM) fiber bundles change dynamically with age. These changes could be driven by alterations in axonal diameter, axonal density, and myelin content. In this study, we applied a novel fixel-based analysis (FBA) framework to examine these changes throughout the adult lifespan. Using diffusion-weighted images from a cohort of 293 healthy volunteers (89 males/204 females) from ages 21 to 86 years old, we performed FBA to analyze age-related changes in microscopic fiber density (FD) and macroscopic fiber morphology (fiber cross section [FC]). Our results showed significant and widespread age-related alterations in FD and FC across the whole brain. Interestingly, some fiber bundles such as the anterior thalamic radiation, corpus callosum, and superior longitudinal fasciculus only showed significant negative relationship with age in FD values, but not in FC. On the other hand, some segments of the cerebello-thalamo-cortical pathway only showed significant negative relationship with age in FC, but not in FD. Analysis at the tract-level also showed that major fiber tract groups predominantly distributed in the frontal lobe (cingulum, forceps minor) exhibited greater vulnerability to the aging process than the others. Differences in FC and the combined measure of FD and cross section values observed between sexes were mostly driven by differences in brain sizes although male participants tended to exhibit steeper negative linear relationship with age in FD as compared to female participants. Overall, these findings provide further insights into the structural changes the brain's WM undergoes due to the aging process.

    DOI: 10.1002/hbm.25008

    PubMed

  2. Psychiatric-disorder-related behavioral phenotypes and cortical hyperactivity in a mouse model of 3q29 deletion syndrome. International journal

    Masayuki Baba, Kazumasa Yokoyama, Kaoru Seiriki, Yuichiro Naka, Kensuke Matsumura, Momoka Kondo, Kana Yamamoto, Misuzu Hayashida, Atsushi Kasai, Yukio Ago, Kazuki Nagayasu, Atsuko Hayata-Takano, Akinori Takahashi, Shun Yamaguchi, Daisuke Mori, Norio Ozaki, Tadashi Yamamoto, Kazuhiro Takuma, Ryota Hashimoto, Hitoshi Hashimoto, Takanobu Nakazawa

    Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology   Vol. 44 ( 12 ) page: 2125 - 2135   2019.11

     More details

    Language:English  

    3q29 microdeletion, a rare recurrent copy number variant (CNV), greatly confers an increased risk of psychiatric disorders, such as schizophrenia and autism spectrum disorder (ASD), as well as intellectual disability. However, disease-relevant cellular phenotypes of 3q29 deletion syndrome remain to be identified. To reveal the molecular and cellular etiology of 3q29 deletion syndrome, we generated a mouse model of human 3q29 deletion syndrome by chromosome engineering, which achieved construct validity. 3q29 deletion (Df/+) mice showed reduced body weight and brain volume and, more importantly, impaired social interaction and prepulse inhibition. Importantly, the schizophrenia-related impaired prepulse inhibition was reversed by administration of antipsychotics. These findings are reminiscent of the growth defects and neuropsychiatric behavioral phenotypes in patients with 3q29 deletion syndrome and exemplify that the mouse model achieves some part of face validity and predictive validity. Unbiased whole-brain imaging revealed that neuronal hyperactivation after a behavioral task was strikingly exaggerated in a restricted region of the cortex of Df/+ mice. We further elucidated the cellular phenotypes of neuronal hyperactivation and the reduction of parvalbumin expression in the cortex of Df/+ mice. Thus, the 3q29 mouse model provides invaluable insight into the disease-causative molecular and cellular pathology of psychiatric disorders.

    DOI: 10.1038/s41386-019-0441-5

    PubMed

  3. MUTATION SCREENING OF THE PCDH15 GENE IN PATIENTS SUFFERING FROM AUTISM SPECTRUM DISORDERS AND SCHIZOPHRENIA

    Ishizuka Kanako, Wang Chenyao, Kimura Hiroki, Xing Jingrui, Kushima Itaru, Arioka Yuko, Yoshimi Akira, Nakamura Yukako, Oya-Ito Tomoko, Takasaki Yuto, Uno Yota, Okada Takashi, Mori Daisuke, Aleksic Branko, Ozaki Norio

    EUROPEAN NEUROPSYCHOPHARMACOLOGY   Vol. 27   page: S162-S163   2017.10

     More details

    Language:English   Publishing type:Rapid communication, short report, research note, etc. (scientific journal)  

  4. IDENTIFICATION OF RARE DISRUPTIVE VARIANTS IN VOLTAGE-GATED CHANNEL GENES (CACNA1C, CACNA1D, CACNA1S, CACNA1I) IN JAPANESE SAMPLES OF SCHIZOPHRENIA AND AUTISM SPECTRUM DISORDER USING ION TORRENT PGM PLATFORM

    Chenyao Wang, Hiroki Kimura, Jingrui Xing, Kanoko Ishizuka, Itaru Kushima, Yuko Arioka, Akira Yoshimi, Yukako Nakamura, Yomoko Shiino, Yuko Oya, Yuto Takasaki, Branko Aleksic, Daisuke Mori, Norio Ozaki

    EUROPEAN NEUROPSYCHOPHARMACOLOGY   Vol. 27   page: S341 - S342   2017.10

     More details

    Language:English   Publishing type:Research paper, summary (international conference)   Publisher:ELSEVIER SCIENCE BV  

    Web of Science

  5. 統合失調症発症に強い影響を及ぼす、頻度の低い稀な遺伝子変異を22q11.2欠失領域に存在するミエリン関連遺伝子のRTN4Rに同定した

    木村 大樹, 藤田 幸, 川端 猛, 石塚 佳奈子, Wang Chenyao, 岩山 佳美, 岡久 祐子, 久島 周, 宇野 洋太, 岡田 俊, 森川 真子, 森 大輔, 池田 匡志, 稲田 俊也, Aleksic Branko, 吉川 武男, 岩田 仲生, 中村 春木, 山下 俊英, 尾崎 紀夫

    日本生物学的精神医学会・日本神経精神薬理学会合同年会プログラム・抄録集   Vol. 39回・47回   page: 190 - 190   2017.9

     More details

    Language:Japanese   Publisher:日本生物学的精神医学会・日本神経精神薬理学会  

  6. 本邦における統合失調症と自閉スペクトラム症に関連するGRIN2Bの遺伝子変異の探索

    高崎 悠登, 尾崎 紀夫, 小出 隆義, 王 晨堯, 木村 大樹, 久島 周, 石塚 佳奈子, 森 大輔, 池田 匡志, アレクシッチ・ブランコ, 岡田 俊, 江川 純, 桑原 斉, 染矢 俊幸, 吉川 武男, 岩田 仲生

    精神神経学雑誌   ( 2017特別号 ) page: S626 - S626   2017.6

     More details

    Language:Japanese   Publisher:(公社)日本精神神経学会  

  7. 統合失調症発症に強い影響を及ぼす、頻度の低い稀な遺伝子変異を22q11.2欠失領域に存在するミエリン関連遺伝子のRTN4Rに同定した

    木村 大樹, 尾崎 紀夫, 藤田 幸, 川端 猛, 石塚 佳奈子, Wang Chenyao, 岩山 佳美, 岡久 祐子, 久島 周, 森川 真子, 宇野 洋太, 岡田 俊, 森 大輔, 池田 匡志, 稲田 俊也, Aleksic Branko, 吉川 武男, 岩田 仲生, 中村 春木, 山下 俊英

    精神神経学雑誌   ( 2017特別号 ) page: S622 - S622   2017.6

     More details

    Language:Japanese   Publisher:(公社)日本精神神経学会  

  8. 本邦における統合失調症と自閉スペクトラム症に関連するGRIN2Bの遺伝子変異の探索

    高崎 悠登, 尾崎 紀夫, 小出 隆義, 王 晨堯, 木村 大樹, 久島 周, 石塚 佳奈子, 森 大輔, 池田 匡志, アレクシッチ・ブランコ, 岡田 俊, 江川 純, 桑原 斉, 染矢 俊幸, 吉川 武男, 岩田 仲生

    精神神経学雑誌   ( 2017特別号 ) page: S626 - S626   2017.6

     More details

    Language:Japanese   Publisher:(公社)日本精神神経学会  

▼display all

KAKENHI (Grants-in-Aid for Scientific Research) 2

  1. Molecular biological analysis of BTEB2

      More details

    Grant type:Competitive

  2. 細胞分裂における中心体生化学的解析

      More details

    Grant type:Competitive

 

Teaching Experience (Off-campus) 4

  1. 基礎医学セミナー

    Nagoya University)

  2. Biochemistry

    Osaka-City University)

  3. Basic training course of medical research

    Nagoya Univercity)

  4. 生化学

    Osaka City University)