Updated on 2025/04/01

写真a

 
KATO Hidekazu
 
Organization
Graduate School of Medicine Department of Clinical Psychiatry Endowed Chair Designated lecturer
Title
Designated lecturer
External link

Degree 1

  1. 博士(医学) ( 2021.3   名古屋大学 ) 

Research Interests 3

  1. 児童思春期精神医学

  2. 遺伝カウンセリング

  3. 自閉スペクトラム症

Current Research Project and SDGs 1

  1. 精神障害をもつ患者でのヒストンメチル化修飾の調節障害

Education 2

  1. Nagoya University

    - 2021.3

  2. University of Toyama

    - 2007.3

Committee Memberships 3

  1. 愛知児童青年精神医学会   評議員  

    2024   

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    Committee type:Academic society

  2. 日本児童青年精神医学会   評議員  

    2024   

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    Committee type:Academic society

  3. 日本児童青年精神医学会   生涯教育委員  

    2023   

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    Committee type:Academic society

Awards 3

  1. 国際学会発表賞(シンポジウム組織部門)

    2024.6   日本精神神経学会  

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  2. 国際学会発表奨励賞

    2023.11   日本児童青年精神医学会  

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  3. International Conference Presentation Award

    2016.6   Child and adolescent psychiatry: Overview of training system and update situation in Asian countries(The 22nd International Association for Child and Adolescent Psychiatry and Allied Professions World Congress)

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Papers 22

  1. Whole-genome sequencing analysis of Japanese autism spectrum disorder trios. Reviewed International journal

    Sawako Furukawa, Itaru Kushima, Hidekazu Kato, Hiroki Kimura, Yoshihiro Nawa, Branko Aleksic, Masahiro Banno, Maeri Yamamoto, Mariko Uematsu, Yukako Nagasaki, Tomoo Ogi, Norio Ozaki, Masashi Ikeda

    Psychiatry and clinical neurosciences     2024.11

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

    AIM: Autism spectrum disorder (ASD) is a genetically and phenotypically heterogeneous neurodevelopmental disorder with a strong genetic basis. Conducting the first comprehensive whole-genome sequencing (WGS) analysis of Japanese ASD trios, this study aimed to elucidate the clinical significance of pathogenic variants and enhance the understanding of ASD pathogenesis. METHODS: WGS was performed on 57 Japanese patients with ASD and their parents, investigating variants ranging from single-nucleotide variants to structural variants (SVs), short tandem repeats (STRs), mitochondrial variants, and polygenic risk score (PRS). RESULTS: Potentially pathogenic variants that could explain observed phenotypes were identified in 18 patients (31.6%) overall and in 10 of 23 patients (43.5%) with comorbid intellectual developmental disorder (IDD). De novo variants in PTEN, CHD7, and HNRNPH2 were identified in patients referred for genetic counseling who exhibited previously reported phenotypes, including one patient with ASD who had profound IDD and macrocephaly with PTEN L320S. Analysis of the AlphaFold3 protein structure indicated potential inhibition of intramolecular interactions within PTEN. SV analysis identified deletions in ARHGAP11B and TMLHE. A pathogenic de novo mitochondrial variant was identified in a patient with ASD who had a history of encephalitis and cognitive decline. GO enrichment analysis of genes with nonsense variants and missense variants (Missense badness, PolyPhen-2, and Constraint >1) showed associations with regulation of growth and ATP-dependent chromatin remodeler activity. No reportable results were obtained in the analysis of STR and PRS. CONCLUSION: Characterizing the comprehensive genetic architecture and phenotypes of ASD is a fundamental step towards unraveling its complex biology.

    DOI: 10.1111/pcn.13767

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  2. Copy number variations in RNF216 and postsynaptic membrane-associated genes are associated with bipolar disorder: a case-control study in the Japanese population. Reviewed International journal

    Masahiro Nakatochi, Itaru Kushima, Branko Aleksic, Hiroki Kimura, Hidekazu Kato, Toshiya Inada, Youta Torii, Nagahide Takahashi, Maeri Yamamoto, Kunihiro Iwamoto, Yoshihiro Nawa, Shuji Iritani, Nakao Iwata, Takeo Saito, Kohei Ninomiya, Tomo Okochi, Ryota Hashimoto, Hidenaga Yamamori, Yuka Yasuda, Michiko Fujimoto, Kenichiro Miura, Kazutaka Ohi, Toshiki Shioiri, Kiyoyuki Kitaichi, Masanari Itokawa, Makoto Arai, Mitsuhiro Miyashita, Kazuya Toriumi, Tsutomu Takahashi, Michio Suzuki, Takahiro A Kato, Shigenobu Kanba, Hideki Horikawa, Kiyoto Kasai, Tempei Ikegame, Seiichiro Jinde, Tadafumi Kato, Chihiro Kakiuchi, Bun Yamagata, Shintaro Nio, Yasuto Kunii, Hirooki Yabe, Yasunobu Okamura, Shu Tadaka, Ueno Fumihiko, Taku Obara, Yasuyuki Yamamoto, Yuko Arioka, Daisuke Mori, Masashi Ikeda, Norio Ozaki

    Psychiatry and clinical neurosciences     2024.10

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    AIM: Bipolar disorder (BD) is a common psychiatric disorder characterized by alterations between manic/hypomanic and depressive states. Rare pathogenic copy number variations (CNVs) that overlap with exons of synaptic genes have been associated with BD. However, no study has comprehensively explored CNVs in synaptic genes associated with BD. Here, we evaluated the relationship between BD and rare CNVs that overlap with synaptic genes, not limited to exons, in the Japanese population. METHODS: Using array comparative genome hybridization, we detected CNVs in 1839 patients with BD and 2760 controls. We used the Synaptic Gene Ontology database to identify rare CNVs that overlap with synaptic genes. Using gene-based analysis, we compared their frequencies between the BD and control groups. We also searched for synaptic gene sets related to BD. The significance level was set to a false discovery rate of 10%. RESULTS: The RNF216 gene was significantly associated with BD (odds ratio, 4.51 [95% confidence interval, 1.66-14.89], false discovery rate < 10%). The BD-associated CNV that corresponded with RNF216 also partially overlapped with the minimal critical region of the 7p22.1 microduplication syndrome. The integral component of the postsynaptic membrane (Gene Ontology:0099055) was significantly associated with BD. The CNV overlapping with the intron region of GRM5 in this gene set showed a nominal significant association between cases and controls (P < 0.05). CONCLUSION: We provide evidence that CNVs in RNF216 and postsynaptic membrane-related genes confer a risk of BD, contributing to a better understanding of the pathogenesis of BD.

    DOI: 10.1111/pcn.13752

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  3. Treatment-resistant schizophrenia with 22q11.2 deletion and additional genetic defects. Reviewed International journal

    Sawako Furukawa, Shusei Arafuka, Hidekazu Kato, Tomoo Ogi, Norio Ozaki, Masashi Ikeda, Itaru Kushima

    Neuropsychopharmacology reports     2024.8

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

    We report a case of a 61-year-old female with 22q11.2 deletion syndrome (22q11.2DS) and a novel heterozygous nonsense variant in MAP1A, identified through whole-genome sequencing (WGS). The patient presented with intellectual developmental disorder, treatment-resistant schizophrenia (SCZ), and multiple congenital anomalies. Despite aggressive pharmacotherapy, she experienced persistent auditory hallucinations and negative symptoms. WGS revealed a 3 Mb deletion at 22q11.2 and a nonsense variant in MAP1A (c.4652T>G, p.Leu1551*). MAP1A, encoding microtubule-associated protein 1A, is crucial for axon and dendrite development and has been implicated in autism spectrum disorder and SCZ. The MAP1A variant may contribute to the severe psychiatric phenotype, as it is thought to influence synaptic plasticity, a process also affected by 22q11.2 deletion. This case highlights the importance of WGS in identifying additional pathogenic variants that may explain phenotypic variability in 22q11.2DS. Thus, WGS can lead to a better understanding of the genetic architecture of 22q11.2DS. However, further studies are needed to elucidate the role of secondary genetic contributors in the diverse clinical presentations of 22q11.2DS.

    DOI: 10.1002/npr2.12477

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  4. Analysis of human neuronal cells carrying ASTN2 deletion associated with psychiatric disorders. Reviewed International journal

    Yu Hayashi, Hiroki Okumura, Yuko Arioka, Itaru Kushima, Daisuke Mori, Tzuyao Lo, Gantsooj Otgonbayar, Hidekazu Kato, Yoshihiro Nawa, Hiroki Kimura, Branko Aleksic, Norio Ozaki

    Translational psychiatry   Vol. 14 ( 1 ) page: 236 - 236   2024.6

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

    Recent genetic studies have found common genomic risk variants among psychiatric disorders, strongly suggesting the overlaps in their molecular and cellular mechanism. Our research group identified the variant in ASTN2 as one of the candidate risk factors across these psychiatric disorders by whole-genome copy number variation analysis. However, the alterations in the human neuronal cells resulting from ASTN2 variants identified in patients remain unknown. To address this, we used patient-derived and genome-edited iPS cells with ASTN2 deletion; cells were further differentiated into neuronal cells. A comprehensive gene expression analysis using genome-edited iPS cells with variants on both alleles revealed that the expression level of ZNF558, a gene specifically expressed in human forebrain neural progenitor cells, was greatly reduced in ASTN2-deleted neuronal cells. Furthermore, the expression of the mitophagy-related gene SPATA18, which is repressed by ZNF558, and mitophagy activity were increased in ASTN2-deleted neuronal cells. These phenotypes were also detected in neuronal cells differentiated from patient-derived iPS cells with heterozygous ASTN2 deletion. Our results suggest that ASTN2 deletion is related to the common pathogenic mechanism of psychiatric disorders by regulating mitophagy via ZNF558.

    DOI: 10.1038/s41398-024-02962-4

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  5. Study of the genetic association between selected 3q29 region genes and schizophrenia and autism spectrum disorder in the Japanese population. Reviewed

    Gantsooj Otgonbayar, Tzuyao Lo, Yu Hayashi, Sho Furuta, Branko Aleksic, Yoshihiro Nawa, Itaru Kushima, Hidekazu Kato, Hiroki Kimura, Norio Ozaki

    Nagoya journal of medical science   Vol. 86 ( 2 ) page: 216 - 222   2024.5

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

    Psychiatric disorders are highly inheritable, and most psychiatric disorders exhibit genetic overlap. Recent studies associated the 3q29 recurrent deletion with schizophrenia (SCZ) and autism spectrum disorder (ASD). In this study, we investigated the association of genes in the 3q29 region with SCZ and ASD. TM4SF19 and PAK2 were chosen as candidate genes for this study based on evidence from previous research. We sequenced TM4SF19 and PAK2 in 437 SCZ cases, 187 ASD cases and 524 controls in the Japanese population. Through targeted sequencing, we identified 6 missense variants among the cases (ASD & SCZ), 3 missense variants among controls, and 1 variant common to both cases and controls; however, no loss-of-function variants were identified. Fisher's exact test showed a significant association of variants in TM4SF19 among cases (p=0.0160). These results suggest TM4SF19 variants affect the etiology of SCZ and ASD in the Japanese population. Further research examining 3q29 region genes and their association with SCZ and ASD is thus needed.

    DOI: 10.18999/nagjms.86.2.216

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MISC 20

  1. Launching a child and adolescent psychiatry training program in Mongolia inspired by Japanese models

    Khishigsuren Zuunnast, Hidekazu Kato, Kana Yokoyama, Yoshihiro Nawa, Shiori Ogawa, Toru Yoshikawa, Hitoshi Kaneko, Masako Nagata, Oyunsuren Davaasuren, Kenji Nomura

    Psychiatry and Clinical Neurosciences Reports   Vol. 4 ( 1 )   2025.3

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

    DOI: 10.1002/pcn5.70056

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  2. 子どもの眠りに影響する薬剤―OTC薬を含めて

    加藤 秀一, 大野 由佳, 高橋 長秀

    小児内科   Vol. 56 ( 8 ) page: 1191 - 1196   2024.8

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  3. 【発達障害を支援する】発達障害の遺伝学的研究 自閉スペクトラム症を中心に

    加藤 秀一

    カレントテラピー   Vol. 42 ( 7 ) page: 568 - 572   2024.7

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    Language:Japanese   Publisher:(株)ライフメディコム  

    自閉スペクトラム症(ASD)はじめ,いわゆる発達障害(神経発達症)の背景には多様な病態が含まれることが想定されるが,いまだその詳細は不明である.神経発達症のなかでもASDと注意欠如多動症において,遺伝要因の影響が比較的に大きいことが知られている.ASDでは影響力の大きな病的意義のあるゲノムバリアントが多数報告され,多くのASD関連遺伝子が報告され,関連遺伝子には遺伝子発現の調整に関わる遺伝子や神経伝達に関わる遺伝子が多いことなどが明らかにされてきた.これらゲノムバリアントや見出された関連遺伝子を起点として,病態解明のための研究が進められている.また,本邦でも染色体のコピー数バリアントを同定するためのマイクロアレイ染色体検査が保険適用となるなど,医療においてゲノム情報の活用が進むなか,神経発達症に関する適切な遺伝カウンセリングが求められている.(著者抄録)

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  4. Psychiatric Lecture 成因・危険因子 ゲノムコピー数バリアントに着目した重症摂食症の病因解析

    久島 周, 今枝 美穂, 田中 聡, 加藤 秀一, 大矢 友子, 中杤 昌弘, アレクシッチ・ブランコ, 尾崎 紀夫

    精神科臨床Legato   Vol. 10 ( 1 ) page: 18 - 21   2024.4

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    Language:Japanese   Publisher:(株)メディカルレビュー社  

    摂食症の発症には遺伝的要因が関与することが知られている。筆者らは,重症の摂食症患者を対象にゲノムコピー数バリアント(CNV)解析を行った結果,神経発達症に関連するCNVが発症リスクに関与すること,摂食症病態にシナプス機能異常が寄与することが示唆された。この知見に基づき,今後,分子メカニズムの解明が進むことが期待される。(著者抄録)

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  5. てんかんの患者が利用できる社会福祉制度について

    後藤紋香, 加藤秀一, 稲田俊也

    現代医学   Vol. 69 ( 2 ) page: 60 - 65   2022.12

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Presentations 30

  1. COVID-19罹患後に飲食、歩行、会話、セルフケアを拒絶するようになり、広汎性拒絶症候群の診断に至った男児の1例

    竹中加奈, 松岡崇史, 名和佳弘, 加藤秀一

    愛知児童青年精神医学会第16回学術総会  2025.3.2 

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    Event date: 2025.3

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:名古屋  

  2. 児童精神科での短期研修を行った若手小児科医師へのアンケート調査

    加藤秀一, 松田慶子, 高橋長秀, 名和佳弘

    第132回日本小児精神神経学会  2024.12.1 

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    Event date: 2024.11 - 2024.12

    Language:Japanese   Presentation type:Oral presentation (general)  

  3. 摂食障害(神経性やせ症、回避・制限性食物摂取症)の入院治療(生涯教育に関する委員会セミナー「摂食障害を学ぶ」) Invited

    加藤秀一

    第65回日本児童青年精神医学会  2024.10.17 

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    Event date: 2024.10

    Language:Japanese   Presentation type:Public lecture, seminar, tutorial, course, or other speech  

  4. 小児科診療から児童精神科入院治療への連係に時間を要した神経性やせ症の1例

    冨田伊吹季、加藤秀一、高橋長秀

    愛知児童青年精神医学会第15回学術総会  2024.3.10  愛知児童青年精神医学会

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    Event date: 2024.3

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:豊橋  

  5. 回避/制限性食物摂取症の疑いで治療中に神経性やせ症の診断に変更した1例

    鯉江由晴、加藤秀一、高橋長秀

    愛知児童青年精神医学会第15回学術総会  2024.3.10  愛知児童青年精神医学会

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    Event date: 2024.3

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:豊橋  

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

  1. 精神障害の病態としてのヒストンメチル化異常ー患者におけるゲノム変異を起点としてー

    Grant number:22K15748  2022.4 - 2025.3

    日本学術振興会  科学研究費助成事業 若手研究  若手研究

    加藤 秀一

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  2. Dysregulation of Histone Methylation Modification in Patients with Psychiatric Disorders

    Grant number:21K20866  2021.8 - 2023.3

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research Grant-in-Aid for Research Activity Start-up  Grant-in-Aid for Research Activity Start-up

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    Authorship:Principal investigator 

    Grant amount:\3120000 ( Direct Cost: \2400000 、 Indirect Cost:\720000 )

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Teaching Experience (On-campus) 3

  1. PBLチュートリアル

    2024

  2. PBLチュートリアル

    2022

  3. PBLチュートリアル

    2021

 

Social Contribution 8

  1. 愛知県自閉症協会・つぼみの会 相談会

    Role(s):Advisor

    愛知県自閉症協会・つぼみの会  2025.1

  2. 愛知県てんかん治療医療連携協議会 委員

    Role(s):Organizing member

    愛知県  2024.4

  3. 愛知県自閉症協会・つぼみの会 相談会

    Role(s):Advisor

    愛知県自閉症協会・つぼみの会  2024.2

  4. 愛知県青い鳥医療療育センター 地域療育研修会

    Role(s):Lecturer

    愛知県青い鳥医療療育センター  2023.9

  5. モンゴル国における子どものこころの診療を行うことの出来る医師の養成事業

    Role(s):Lecturer, Organizing member

    2023

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