医学部
  1. 研究者リスト
  2. 齋藤 竹生

齋藤 竹生

saito takeo

基本情報

所属
藤田医科大学 医学部 医学科 精神神経科学 講師
学位
医学博士(藤田医科大学)
J-GLOBAL ID
201501001954870181
researchmap会員ID
7000013117

研究分野

 1

経歴

 3

学歴

 2

受賞

 5

論文

 54
  • Sarah M C Colbert, Lauren Lepow, Brian Fennessy, Nakao Iwata, Masashi Ikeda, Takeo Saito, Chikashi Terao, Michael Preuss, Jyotishman Pathak, J John Mann, Hilary Coon, Niamh Mullins
    Translational psychiatry 15(1) 63-63 2025年2月20日  
    Suicidal ideation (SI) and behavior (SB) are major public health concerns, but risk factors for their development and progression are poorly understood. We used ICD codes and a natural language processing algorithm to identify individuals in a hospital biobank with SI-only, SB, and controls without either. We compared the profiles of SB and SI-only patients to controls, and each other, using phenome-wide association studies (PheWAS) and polygenic risk scores (PRS). PheWAS identified many risk factors for SB and SI-only, plus specific psychiatric disorders which may be involved in progression from SI-only to SB. PRS for suicide attempt were only associated with SB, and even after accounting for psychiatric disorder PRS. SI PRS were only associated with SI-only, although not after accounting for psychiatric disorder PRS. These findings advance understanding of distinct genetic and clinical risk factors for SB and SI-only, which will aid in early detection and intervention efforts.
  • Kevin S O'Connell, Maria Koromina, Tracey van der Veen, Toni Boltz, Friederike S David, Jessica Mei Kay Yang, Keng-Han Lin, Xin Wang, Jonathan R I Coleman, Brittany L Mitchell, Caroline C McGrouther, Aaditya V Rangan, Penelope A Lind, Elise Koch, Arvid Harder, Nadine Parker, Jaroslav Bendl, Kristina Adorjan, Esben Agerbo, Diego Albani, Silvia Alemany, Ney Alliey-Rodriguez, Thomas D Als, Till F M Andlauer, Anastasia Antoniou, Helga Ask, Nicholas Bass, Michael Bauer, Eva C Beins, Tim B Bigdeli, Carsten Bøcker Pedersen, Marco P Boks, Sigrid Børte, Rosa Bosch, Murielle Brum, Ben M Brumpton, Nathalie Brunkhorst-Kanaan, Monika Budde, Jonas Bybjerg-Grauholm, William Byerley, Judit Cabana-Domínguez, Murray J Cairns, Bernardo Carpiniello, Miquel Casas, Pablo Cervantes, Chris Chatzinakos, Hsi-Chung Chen, Tereza Clarence, Toni-Kim Clarke, Isabelle Claus, Brandon Coombes, Elizabeth C Corfield, Cristiana Cruceanu, Alfredo Cuellar-Barboza, Piotr M Czerski, Konstantinos Dafnas, Anders M Dale, Nina Dalkner, Franziska Degenhardt, J Raymond DePaulo, Srdjan Djurovic, Ole Kristian Drange, Valentina Escott-Price, Ayman H Fanous, Frederike T Fellendorf, I Nicol Ferrier, Liz Forty, Josef Frank, Oleksandr Frei, Nelson B Freimer, John F Fullard, Julie Garnham, Ian R Gizer, Scott D Gordon, Katherine Gordon-Smith, Tiffany A Greenwood, Jakob Grove, José Guzman-Parra, Tae Hyon Ha, Tim Hahn, Magnus Haraldsson, Martin Hautzinger, Alexandra Havdahl, Urs Heilbronner, Dennis Hellgren, Stefan Herms, Ian B Hickie, Per Hoffmann, Peter A Holmans, Ming-Chyi Huang, Masashi Ikeda, Stéphane Jamain, Jessica S Johnson, Lina Jonsson, Janos L Kalman, Yoichiro Kamatani, James L Kennedy, Euitae Kim, Jaeyoung Kim, Sarah Kittel-Schneider, James A Knowles, Manolis Kogevinas, Thorsten M Kranz, Kristi Krebs, Steven A Kushner, Catharina Lavebratt, Jacob Lawrence, Markus Leber, Heon-Jeong Lee, Calwing Liao, Susanne Lucae, Martin Lundberg, Donald J MacIntyre, Wolfgang Maier, Adam X Maihofer, Dolores Malaspina, Mirko Manchia, Eirini Maratou, Lina Martinsson, Manuel Mattheisen, Nathaniel W McGregor, Melvin G McInnis, James D McKay, Helena Medeiros, Andreas Meyer-Lindenberg, Vincent Millischer, Derek W Morris, Paraskevi Moutsatsou, Thomas W Mühleisen, Claire O'Donovan, Catherine M Olsen, Georgia Panagiotaropoulou, Sergi Papiol, Antonio F Pardiñas, Hye Youn Park, Amy Perry, Andrea Pfennig, Claudia Pisanu, James B Potash, Digby Quested, Mark H Rapaport, Eline J Regeer, John P Rice, Margarita Rivera, Eva C Schulte, Fanny Senner, Alexey Shadrin, Paul D Shilling, Engilbert Sigurdsson, Lisa Sindermann, Lea Sirignano, Dan Siskind, Claire Slaney, Laura G Sloofman, Olav B Smeland, Daniel J Smith, Janet L Sobell, Maria Soler Artigas, Dan J Stein, Frederike Stein, Mei-Hsin Su, Heejong Sung, Beata Świątkowska, Chikashi Terao, Markos Tesfaye, Martin Tesli, Thorgeir E Thorgeirsson, Jackson G Thorp, Claudio Toma, Leonardo Tondo, Paul A Tooney, Shih-Jen Tsai, Evangelia Eirini Tsermpini, Marquis P Vawter, Helmut Vedder, Annabel Vreeker, James T R Walters, Bendik S Winsvold, Stephanie H Witt, Hong-Hee Won, Robert Ye, Allan H Young, Peter P Zandi, Lea Zillich, Rolf Adolfsson, Martin Alda, Lars Alfredsson, Lena Backlund, Bernhard T Baune, Frank Bellivier, Susanne Bengesser, Wade H Berrettini, Joanna M Biernacka, Michael Boehnke, Anders D Børglum, Gerome Breen, Vaughan J Carr, Stanley Catts, Sven Cichon, Aiden Corvin, Nicholas Craddock, Udo Dannlowski, Dimitris Dikeos, Bruno Etain, Panagiotis Ferentinos, Mark Frye, Janice M Fullerton, Micha Gawlik, Elliot S Gershon, Fernando S Goes, Melissa J Green, Maria Grigoroiu-Serbanescu, Joanna Hauser, Frans A Henskens, Jens Hjerling-Leffler, David M Hougaard, Kristian Hveem, Nakao Iwata, Ian Jones, Lisa A Jones, René S Kahn, John R Kelsoe, Tilo Kircher, George Kirov, Po-Hsiu Kuo, Mikael Landén, Marion Leboyer, Qingqin S Li, Jolanta Lissowska, Christine Lochner, Carmel Loughland, Jurjen J Luykx, Nicholas G Martin, Carol A Mathews, Fermin Mayoral, Susan L McElroy, Andrew M McIntosh, Francis J McMahon, Sarah E Medland, Ingrid Melle, Lili Milani, Philip B Mitchell, Gunnar Morken, Ole Mors, Preben Bo Mortensen, Bertram Müller-Myhsok, Richard M Myers, Woojae Myung, Benjamin M Neale, Caroline M Nievergelt, Merete Nordentoft, Markus M Nöthen, John I Nurnberger, Michael C O'Donovan, Ketil J Oedegaard, Tomas Olsson, Michael J Owen, Sara A Paciga, Christos Pantelis, Carlos N Pato, Michele T Pato, George P Patrinos, Joanna M Pawlak, Josep Antoni Ramos-Quiroga, Andreas Reif, Eva Z Reininghaus, Marta Ribasés, Marcella Rietschel, Stephan Ripke, Guy A Rouleau, Panos Roussos, Takeo Saito, Ulrich Schall, Martin Schalling, Peter R Schofield, Thomas G Schulze, Laura J Scott, Rodney J Scott, Alessandro Serretti, Jordan W Smoller, Alessio Squassina, Eli A Stahl, Hreinn Stefansson, Kari Stefansson, Eystein Stordal, Fabian Streit, Patrick F Sullivan, Gustavo Turecki, Arne E Vaaler, Eduard Vieta, John B Vincent, Irwin D Waldman, Cynthia S Weickert, Thomas W Weickert, Thomas Werge, David C Whiteman, John-Anker Zwart, Howard J Edenberg, Andrew McQuillin, Andreas J Forstner, Niamh Mullins, Arianna Di Florio, Roel A Ophoff, Ole A Andreassen
    Nature 2025年1月22日  
    Bipolar disorder is a leading contributor to the global burden of disease1. Despite high heritability (60-80%), the majority of the underlying genetic determinants remain unknown2. We analysed data from participants of European, East Asian, African American and Latino ancestries (n = 158,036 cases with bipolar disorder, 2.8 million controls), combining clinical, community and self-reported samples. We identified 298 genome-wide significant loci in the multi-ancestry meta-analysis, a fourfold increase over previous findings3, and identified an ancestry-specific association in the East Asian cohort. Integrating results from fine-mapping and other variant-to-gene mapping approaches identified 36 credible genes in the aetiology of bipolar disorder. Genes prioritized through fine-mapping were enriched for ultra-rare damaging missense and protein-truncating variations in cases with bipolar disorder4, highlighting convergence of common and rare variant signals. We report differences in the genetic architecture of bipolar disorder depending on the source of patient ascertainment and on bipolar disorder subtype (type I or type II). Several analyses implicate specific cell types in the pathophysiology of bipolar disorder, including GABAergic interneurons and medium spiny neurons. Together, these analyses provide additional insights into the genetic architecture and biological underpinnings of bipolar disorder.
  • 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 79(1) 12-20 2025年1月  
    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.
  • Takuma Ashizawa, Takeo Saito, Tomo Okochi, Kohei Ninomiya, Kenta Ito, Rei Aoki, Masashi Ikeda, Nakao Iwata
    Translational Psychiatry 14(1) 2024年10月14日  
    Abstract Recent genome-wide association studies (GWASs) have identified fatty acid desaturase (FADS) genes, which code key enzymes involved in polyunsaturated fatty acid (PUFA) desaturation as susceptibility genes for bipolar disorder (BD). Several quantitative changes in PUFAs suggest their involvement in BD pathogenesis. Therefore, this study aimed to clarify the relationship between BD and PUFAs by conducting lipidomics covariating with the FADS gene variant (rs174550), which is associated with PUFA levels and BD susceptibility. The concentrations of 23 fatty acids were measured using plasma samples from the BD group (n = 535) and the control group (n = 107). Differences in each PUFA concentration ratio were compared between the two groups. Also, differences in each PUFA concentration ratio were compared for each genotype in rs174550. Our results showed that the BD group had significantly lower concentrations of linoleic acid (LA) (β = −0.36, p = 0.023) and arachidonic acid (AA) (β = −0.18, p = 0.013) than the control group. Concerning the effect of FADS on the PUFA concentration ratio, carriers of C-allele at rs174550 had significantly decreased γ-linolenic acid and AA concentration ratios. A previous GWAS reported that the presence of a C-allele at rs174550 increased the BD risk. This direction is consistent with the lipidomic results of the present study. In conclusion, both the FADS and BD were considered to regulate the AA concentration. Thus, as the FADS gene variant is crucial for conducting lipidomics of BD we believe that the allele frequency of FADS must be analyzed.
  • Satoshi Koyama, Xiaoxi Liu, Yoshinao Koike, Keiko Hikino, Masaru Koido, Wei Li, Kotaro Akaki, Kohei Tomizuka, Shuji Ito, Nao Otomo, Hiroyuki Suetsugu, Soichiro Yoshino, Masato Akiyama, Kohei Saito, Yuki Ishikawa, Christian Benner, Pradeep Natarajan, Patrick T Ellinor, Taisei Mushiroda, Momoko Horikoshi, Masashi Ikeda, Nakao Iwata, Koichi Matsuda, Shumpei Niida, Kouichi Ozaki, Yukihide Momozawa, Shiro Ikegawa, Osamu Takeuchi, Kaoru Ito, Chikashi Terao
    Nature genetics 56(10) 2027-2035 2024年10月  
    Human genetic variants are associated with many traits through largely unknown mechanisms. Here, combining approximately 260,000 Japanese study participants, a Japanese-specific genotype reference panel and statistical fine-mapping, we identified 4,423 significant loci across 63 quantitative traits, among which 601 were new, and 9,406 putatively causal variants. New associations included Japanese-specific coding, splicing and noncoding variants, exemplified by a damaging missense variant rs730881101 in TNNT2 associated with lower heart function and increased risk for heart failure (P = 1.4 × 10-15 and odds ratio = 4.5, 95% confidence interval = 3.1-6.5). Putative causal noncoding variants were supported by state-of-art in silico functional assays and had comparable effect sizes to coding variants. A plausible example of new mechanisms of causal variants is an enrichment of causal variants in 3' untranslated regions (UTRs), including the Japanese-specific rs13306436 in IL6 associated with pro-inflammatory traits and protection against tuberculosis. We experimentally showed that transcripts with rs13306436 are resistant to mRNA degradation by regnase-1, an RNA-binding protein. Our study provides a list of fine-mapped causal variants to be tested for functionality and underscores the importance of sequencing, genotyping and association efforts in diverse populations.
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MISC

 28
  • 芦澤 琢磨, 伊藤 健太, 二宮 光平, 齋藤 竹生, 池田 匡志, 岩田 仲生
    精神科臨床Legato 7(3) 140-144 2021年12月  
    統合失調症の病態は依然として不明のままであり、現在に至るまでさまざまな切り口から多くの研究がなされてきた。近年、全ゲノム関連研究(genome-wide association study;GWAS)は疾患感受性遺伝子同定に大きく寄与し、病態研究の新たなヒントを与えている。本稿では統合失調症GWASの成果について触れる。(著者抄録)
  • 池田 匡志, 高橋 篤, 鎌谷 洋一郎, 桃沢 幸秀, 齋藤 竹生, 近藤 健治, 島崎 愛夕, 川瀬 康平, 作佐部 太也, 岩山 佳美, 豊田 倫子, 和久田 智靖, 菊池 充, 金原 信久, 山森 英長, 安田 由華, 渡部 雄一郎, 保谷 智史, アレクシッチ ブランコ, 久島 周, 新井 平伊, 高木 学, 服部 功太郎, 功刀 浩, 岡久 祐子, 大沼 徹, 尾崎 紀夫, 染矢 俊幸, 橋本 亮太, 吉川 武男, 久保 充明, 岩田 仲生
    日本臨床精神神経薬理学会・日本神経精神薬理学会合同年会プログラム・抄録集 29回・49回 124-124 2019年10月  
  • 島崎 愛夕, 齋藤 竹生, 大河内 智, 谷口 賢, 二宮 光平, 橋本 亮太, 池田 匡志, 岩田 仲生, CPC-J日本クロザピン薬理ゲノム学コンソーシアム
    精神神経学雑誌 (2019特別号) S467-S467 2019年6月  
  • 菅原 裕子, 村田 唯, 池亀 天平, 嶋永 翔太, 竹岡 優将, 齋藤 竹生, 池田 匡志, 吉川 茜, 西村 文親, 河村 代志也, 垣内 千尋, 佐々木 司, 岩田 仲生, 橋本 衛, 笠井 清登, 加藤 忠史, 文東 美紀, 岩本 和也
    精神神経学雑誌 121(4) 251-258 2019年4月  
    統合失調症(SZ)と双極性障害(BD)は遺伝要因と環境要因を共有することが知られており,複雑な遺伝環境相互作用が発症に関与すると考えられている.ゲノムワイド関連解析の結果,主要な精神疾患のなかでもSZとBDは遺伝要因の重なりが特に大きいことが知られているが,エピゲノム要因の重なりについては十分な検討がなされていない.本研究では,SZで行われた大規模なゲノムワイドメチル化関連解析(MWAS)で同定された上位5ヶ所の候補領域について,BD試料を用いた検討を行った.5ヶ所の候補領域のうち2ヶ所[FAM63B,染色体16番intergenic領域(IR in chr 16)]では,SZと同様に,BDにおいても有意な低メチル化状態が認められ,SZとBDに共通なエピゲノム要因である可能性が示唆された.また,1ヶ所(TBC1D22A)の領域では,SZとは異なり,BDでは健常者に比して有意な高メチル化状態が認められた.今後,BDを対象とした大規模なMWASによって,両疾患におけるエピゲノム要因の類似性や独自性の詳細がさらに明らかとなるであろう.(著者抄録)
  • 菅原 裕子, 村田 唯, 池亀 天平, 嶋永 翔太, 竹岡 優将, 齋藤 竹生, 池田 匡志, 吉川 茜, 西村 文親, 河村 代志也, 垣内 千尋, 佐々木 司, 岩田 仲生, 橋本 衛, 笠井 清登, 加藤 忠史, 文東 美紀, 岩本 和也
    精神神経学雑誌 121(4) 251-258 2019年4月  
    統合失調症(SZ)と双極性障害(BD)は遺伝要因と環境要因を共有することが知られており,複雑な遺伝環境相互作用が発症に関与すると考えられている.ゲノムワイド関連解析の結果,主要な精神疾患のなかでもSZとBDは遺伝要因の重なりが特に大きいことが知られているが,エピゲノム要因の重なりについては十分な検討がなされていない.本研究では,SZで行われた大規模なゲノムワイドメチル化関連解析(MWAS)で同定された上位5ヶ所の候補領域について,BD試料を用いた検討を行った.5ヶ所の候補領域のうち2ヶ所[FAM63B,染色体16番intergenic領域(IR in chr 16)]では,SZと同様に,BDにおいても有意な低メチル化状態が認められ,SZとBDに共通なエピゲノム要因である可能性が示唆された.また,1ヶ所(TBC1D22A)の領域では,SZとは異なり,BDでは健常者に比して有意な高メチル化状態が認められた.今後,BDを対象とした大規模なMWASによって,両疾患におけるエピゲノム要因の類似性や独自性の詳細がさらに明らかとなるであろう.(著者抄録)
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共同研究・競争的資金等の研究課題

 3
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