Updated on 2025/07/02

写真a

 
OHMORI Iori
 
Organization
Faculty of Education Professor
Position
Professor
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Degree

  • 医学博士 ( 1995.3   岡山大学 )

  • 医学 ( 岡山大学 )

Research Interests

  • 記憶・学習

  • ドラベ症候群

  • チオレドキシン

  • 慢性腎臓病

  • CACNA1A

  • てんかん

  • 電位依存性ナトリウムチャネル

  • 発達障害

  • Oxidative stress

  • 神経分子病態学

  • 神経疾患の病態と治療

  • SCN1A

  • 愛着行動

Research Areas

  • Life Science / Embryonic medicine and pediatrics

  • Life Science / Physiology

  • Life Science / Neuroscience-general

  • Life Science / Pathophysiologic neuroscience

  • Life Science / Genetics

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Professional Memberships

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Papers

  • Txn1mutation is a monogenic cause of chronic kidney disease associated with mitochondrial dysfunction in rats

    Iori Ohmori, Mamoru Ouchida, Yoshiko Hada, Haruhito A. Uchida, Shinya Toyokuni, Tomoji Mashimo

    BioRxiv   2023.8

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

    File: 2023.08.14.553187v1.full.pdf

    DOI: 10.1101/2023.08.14.553187

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  • Thioredoxin deficiency increases oxidative stress and causes bilateral symmetrical degeneration in rat midbrain. Reviewed International journal

    Iori Ohmori, Mamoru Ouchida, Hirohiko Imai, Saeko Ishida, Shinya Toyokuni, Tomoji Mashimo

    Neurobiology of disease   175   105921 - 105921   2022.11

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    Authorship:Lead author, Corresponding author   Language:English   Publishing type:Research paper (scientific journal)   Publisher:Elsevier BV  

    Thioredoxin, encoded by Txn1, acts as a critical antioxidant in the defense against oxidative stress by regulating the dithiol/disulfide balance of interacting proteins. The role of thioredoxin in the central nervous system (CNS) is largely unknown. A phenotype-driven study of N-ethyl-N-nitrosourea-mutated rats with wild-running seizures revealed the importance of Txn1 mutations in CNS degeneration. Genetic mapping identified Txn1-F54L in the epileptic rats. The insulin-reducing activity of Txn1-F54L was approximately one-third of that of the wild-type (WT). Bilateral symmetrical vacuolar degeneration in the midbrain, mainly in the thalamus and the inferior colliculus, was observed in the Txn1-F54L rats. The lesions displayed neuronal and oligodendrocytic cell death. Neurons in Txn1-F54L rats showed morphological changes in the mitochondria. Vacuolar degeneration peaked at five weeks of age, and spontaneous repair began at seven weeks. The TUNEL assay showed that fibroblasts derived from homozygotes were susceptible to cell death under oxidative stress. In five-week-old WT rats, energy metabolism in the thalamus was significantly higher than that in the cerebral cortex. In conclusion, in juvenile rats, Txn1 seems to play an essential role in reducing oxidative stress in the midbrains with high energy metabolism.

    File: 2022 Thioredoxin deficiency increases oxidative stress.pdf

    DOI: 10.1016/j.nbd.2022.105921

    PubMed

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  • Novel animal model of combined generalized and focal epilepsy. Reviewed International journal

    Iori Ohmori, Mamoru Ouchida, Masakazu Shinohara, Kiyoka Kobayashi, Saeko Ishida, Tomoji Mashimo

    Epilepsia   63 ( 7 )   e80 - e85   2022.7

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

    Thioredoxin, encoded by Txn1, is a critical antioxidant that protects against oxidative damage by regulating the dithiol/disulfide balance of interacting proteins. We recently discovered the Adem rat, an epileptic rat harboring the Txn1-F54L mutation, characterized by wild running and vacuolar degeneration in the midbrain. This study aimed to characterize the classification of epilepsy in Adem rats. We performed simultaneous video-electroencephalographic recordings, magnetic resonance imaging, neurotransmitter measurements using gas chromatography-mass spectrometry (GC-MS), and immunohistochemistry. Adem rats exhibited absence, tonic, and focal seizures. The type of epilepsy was classified as combined generalized and focal epilepsy. Neurotransmitters in the midbrain and cortex were measured at 3 weeks of age, when neuronal cell death occurs in the midbrain. The results of GC-MS ruled out the dominance of the excitatory system in the midbrain and cortex of Adem rats. Activation of astrocytes and microglia was more pronounced at 5 weeks of age, at which time epileptic seizures occurred frequently. The underlying pathology in Adem rats remains unknown. However, glial cell activation and inflammation may play a significant role in the occurrence of epilepsy.

    File: 2022 Novel animal model of combined generalized and focal epilepsy.pdf

    DOI: 10.1111/epi.17295

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  • ナトリウムチャネル異常とてんかん Invited Reviewed

    大守(川﨑)伊織

    Epilepsy   18 ( 2 )   33 - 40   2024.12

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    Authorship:Lead author   Language:Japanese   Publishing type:Research paper (scientific journal)  

    File: 最終原稿_ナトリウムチャネルとてんかん.pdf

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  • Large-scale animal model study uncovers altered brain pH and lactate levels as a transdiagnostic endophenotype of neuropsychiatric disorders involving cognitive impairment Reviewed

    Hideo Hagihara, Hirotaka Shoji, Satoko Hattori, Giovanni Sala, Yoshihiro Takamiya, Mika Tanaka, Masafumi Ihara, Mihiro Shibutani, Izuho Hatada, Kei Hori, Mikio Hoshino, Akito Nakao, Yasuo Mori, Shigeo Okabe, Masayuki Matsushita, Anja Urbach, Yuta Katayama, Akinobu Matsumoto, Keiichi I Nakayama, Shota Katori, Takuya Sato, Takuji Iwasato, Haruko Nakamura, Yoshio Goshima, Matthieu Raveau, Tetsuya Tatsukawa, Kazuhiro Yamakawa, Noriko Takahashi, Haruo Kasai, Johji Inazawa, Ikuo Nobuhisa, Tetsushi Kagawa, Tetsuya Taga, Mohamed Darwish, Hirofumi Nishizono, Keizo Takao, Kiran Sapkota, Kazutoshi Nakazawa, Tsuyoshi Takagi, Haruki Fujisawa, Yoshihisa Sugimura, Kyosuke Yamanishi, Lakshmi Rajagopal, Nanette Deneen Hannah, Herbert Y Meltzer, Tohru Yamamoto, Shuji Wakatsuki, Toshiyuki Araki, Katsuhiko Tabuchi, Tadahiro Numakawa, Hiroshi Kunugi, Freesia L Huang, Atsuko Hayata-Takano, Hitoshi Hashimoto, Kota Tamada, Toru Takumi, Takaoki Kasahara, Tadafumi Kato, Isabella A Graef, Gerald R Crabtree, Nozomi Asaoka, Hikari Hatakama, Shuji Kaneko, Takao Kohno, Mitsuharu Hattori, Yoshio Hoshiba, Ryuhei Miyake, Kisho Obi-Nagata, Akiko Hayashi-Takagi, Léa J Becker, Ipek Yalcin, Yoko Hagino, Hiroko Kotajima-Murakami, Yuki Moriya, Kazutaka Ikeda, Hyopil Kim, Bong-Kiun Kaang, Hikari Otabi, Yuta Yoshida, Atsushi Toyoda, Noboru H Komiyama, Seth GN Grant, Michiru Ida-Eto, Masaaki Narita, Ken-ichi Matsumoto, Emiko Okuda-Ashitaka, Iori Ohmori, Tadayuki Shimada, Kanato Yamagata, Hiroshi Ageta, Kunihiro Tsuchida, Kaoru Inokuchi, Takayuki Sassa, Akio Kihara, Motoaki Fukasawa, Nobuteru Usuda, Tayo Katano, Teruyuki Tanaka, Yoshihiro Yoshihara, Michihiro Igarashi, Takashi Hayashi, Kaori Ishikawa, Satoshi Yamamoto, Naoya Nishimura, Kazuto Nakada, Shinji Hirotsune, Kiyoshi Egawa, Kazuma Higashisaka, Yasuo Tsutsumi, Shoko Nishihara, Noriyuki Sugo, Takeshi Yagi, Naoto Ueno, Tomomi Yamamoto, Yoshihiro Kubo, Rie Ohashi, Nobuyuki Shiina, Kimiko Shimizu, Sayaka Higo-Yamamoto, Katsutaka Oishi, Hisashi Mori, Tamio Furuse, Masaru Tamura, Hisashi Shirakawa, Daiki X Sato, Yukiko U Inoue, Takayoshi Inoue, Yuriko Komine, Tetsuo Yamamori, Kenji Sakimura, Tsuyoshi Miyakawa

    eLife   12   2024.3

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:eLife Sciences Publications, Ltd  

    Increased levels of lactate, an end-product of glycolysis, have been proposed as a potential surrogate marker for metabolic changes during neuronal excitation. These changes in lactate levels can result in decreased brain pH, which has been implicated in patients with various neuropsychiatric disorders. We previously demonstrated that such alterations are commonly observed in five mouse models of schizophrenia, bipolar disorder, and autism, suggesting a shared endophenotype among these disorders rather than mere artifacts due to medications or agonal state. However, there is still limited research on this phenomenon in animal models, leaving its generality across other disease animal models uncertain. Moreover, the association between changes in brain lactate levels and specific behavioral abnormalities remains unclear. To address these gaps, the International Brain pH Project Consortium investigated brain pH and lactate levels in 109 strains/conditions of 2294 animals with genetic and other experimental manipulations relevant to neuropsychiatric disorders. Systematic analysis revealed that decreased brain pH and increased lactate levels were common features observed in multiple models of depression, epilepsy, Alzheimer’s disease, and some additional schizophrenia models. While certain autism models also exhibited decreased pH and increased lactate levels, others showed the opposite pattern, potentially reflecting subpopulations within the autism spectrum. Furthermore, utilizing large-scale behavioral test battery, a multivariate cross-validated prediction analysis demonstrated that poor working memory performance was predominantly associated with increased brain lactate levels. Importantly, this association was confirmed in an independent cohort of animal models. Collectively, these findings suggest that altered brain pH and lactate levels, which could be attributed to dysregulated excitation/inhibition balance, may serve as transdiagnostic endophenotypes of debilitating neuropsychiatric disorders characterized by cognitive impairment, irrespective of their beneficial or detrimental nature.

    DOI: 10.7554/elife.89376

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    Other Link: https://cdn.elifesciences.org/articles/89376/elife-89376-v1.xml

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Books

  • てんかん,神経変性症および慢性腎臓病モデル動物としてのTxn1遺伝子変異ラットの樹立

    大守伊織, 大内田守, 真下知士, 豊國伸哉

    株式会社医学書院  2024.10 

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    Language:Japanese

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MISC

  • 上を向いて歩こう

    大守(川﨑)伊織

    脳と発達   56 ( 1 )   2024.1

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    Language:Japanese  

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  • Necessity of ICT utilization in genome education: an analysis based on a questionnaire survey of university students

    十川麗美, 野田夕月奈, 鶴田智彦, 花岡有為子, 平沢晃, 隈元謙介, 大守伊織

    日本遺伝カウンセリング学会誌   45 ( 2 )   2024

  • 最先端医療の今 教育学部を中心とした学生教育に対するゲノム医療リテラシー向上の取り組み

    十川 麗美, 野田 夕月奈, 隈元 謙介, 平沢 晃, 大守 伊織

    Medical Science Digest   49 ( 13 )   722 - 723   2023.12

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    Language:Japanese   Publisher:(株)ニュー・サイエンス社  

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  • マイクロアレイ染色体検査にてCharcot-Marie-Tooth病責任領域の重複が認められたMiller-Dieker症候群の遺伝カウンセリング

    十川 麗美, 秋山 倫之, 衛藤 英理子, 二川 摩周, 加藤 芙美乃, 山本 英喜, 平沢 晃, 大守 伊織, 小林 勝弘

    脳と発達   55 ( Suppl. )   S302 - S302   2023.5

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    Language:Japanese   Publisher:(一社)日本小児神経学会  

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  • Questionnaire survey on information transfer during disasters and emergencies among the hearing impaired

    Questionnaire survey on information, ransfer during disasters, emergencies among the hearing impaired

    27   398 - 398   2023.4

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Presentations

  • Pathophysiological basis of chronic kidney disease due to Txn1 mutation

    2025.3.19 

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    Event date: 2025.3.17 - 2025.3.19

    Language:English   Presentation type:Poster presentation  

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  • 酸化ストレス障害による神経変性と修復過程におけるグリア細胞の役割

    大守伊織

    第66回日本小児神経学会学術集会  2024.5.30 

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    Event date: 2024.5.29 - 2024.6.1

    Language:Japanese   Presentation type:Symposium, workshop panel (nominated)  

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  • Txn1遺伝子変異ラットにおける慢性腎臓病は、ミトコンドリア異常と複数の細胞死パスウェイが関与する

    大守伊織、大内田 守、秦 昌紫子、内田 治仁、豊國 伸哉、真下 知士

    第34回腎とフリーラジカル研究会  2023.11.11 

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    Event date: 2023.11.11

    Language:Japanese   Presentation type:Oral presentation (general)  

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  • 聴覚障害者における災害時・緊急時の情報伝達に関するアンケート調査

    野田夕月奈, 大守伊織, 牧尉太, 片岡祐子

    第28回日本災害医学会総会・学術集会  2023.3 

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    Event date: 2023.3.9 - 2023.3.11

    Language:Japanese   Presentation type:Poster presentation  

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  • A Txn1 missense mutation links to epilepsy with vacuolar degeneration

    Ohmori I, Ouchida M, Toyokuni S, Ishida S, Mashimo T

    39th Congress of the International Union of Physiological Sciences (IUPS)  2022.5.7 

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    Event date: 2022.5.7 - 2022.5.11

    Language:English   Presentation type:Poster presentation  

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Industrial property rights

  • 遺伝子改変非ヒトモデル動物

    大守 伊織, 大内田 守, 真下 知士

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    Applicant:真下 知士

    Application no:JP2018045008  Date applied:2018.12.6

    Publication no:WO2019-117022  Date published:2019620

    J-GLOBAL

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  • 遺伝子改変非ヒトモデル動物

    大守 伊織, 大内田 守, 真下 知士

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    Applicant:大守 伊織

    Application no:特願2019-514326  Date applied:2018.12.6

    Patent/Registration no:特許第6650649号  Date registered:2020.1.23 

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  • 抗てんかん薬

    大守 伊織, 大内田 守

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    Applicant:大守 伊織

    Application no:特願2018-188510  Date applied:2018.10.3

    Announcement no:特開2018-203782  Date announced:2018.12.27

    Patent/Registration no:特許第6587299号  Date registered:2019.9.20 

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  • 抗てんかん薬

    大守 伊織, 大内田 守

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    Applicant:大守 伊織

    Application no:特願2018-188510  Date applied:2018.10.3

    Announcement no:特開2018-203782  Date announced:2018.12.27

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  • てんかん波を伴う疾患治療剤

    大内田 守, 大守 伊織, 改田 祐子

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    Applicant:国立大学法人 岡山大学

    Application no:特願2015-154053  Date applied:2015.8.4

    Announcement no:特開2015-227365  Date announced:2015.12.17

    Patent/Registration no:特許第6158868号  Date registered:2017.6.16 

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Awards

  • 優秀演題賞

    2018.5   日本酸化ストレス学会  

    大守伊織

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  • Gold Poster賞

    2013.6   国際てんかん学会  

    大守伊織

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  • 新見賞

    2009.6   岡山医学会  

    大守伊織

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  • Juhn and Mary Wada奨励賞

    2007.11   日本てんかん学会  

    大守伊織

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  • てんかん治療研究振興財団研究褒賞

    2007.3  

    大守伊織、大内田守

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Research Projects

  • 多様性を尊重する社会の確立を目指した遺伝学リテラシーからの教育実践研究

    2023.04 - 2026.03

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    Authorship:Principal investigator 

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  • Multilayered Omics for Oxidative Stress Induced Neuronal Cell Death and Epileptogenesis

    Grant number:22K07914  2022.04 - 2025.03

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)  Grant-in-Aid for Scientific Research (C)

    大守 伊織, 大内田 守

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    Grant amount:\4160000 ( Direct expense: \3200000 、 Indirect expense:\960000 )

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  • 抗腫瘍剤の開発

    2020.04 - 2022.03

    橋渡し研究推進戦略的プログラム 

    大内田守, 大守伊織

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    Authorship:Coinvestigator(s) 

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  • Study of the pathogenesis of west syndrome using a new model rat

    Grant number:16H05354  2016.04 - 2020.03

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (B)

    Ouchida Mamoru

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    Grant amount:\17030000 ( Direct expense: \13100000 、 Indirect expense:\3930000 )

    On the study of mutant rats established by ENU mutagenesis, we found a lineage of diseased rats with developmental and epileptic encephalopathy-like epilepsy. Epileptic seizures occurred during a limited period of 4 to 6 weeks of age. The brain lesions were recovered spontaneously. The causative gene found in the rats is a missense mutation of a gene that regulates oxidative stress by redox reaction. Our results suggested that there may be a critical period when the oxidative stress becomes particularly high in the local region of the brain during the developmental process of the brain. Mutant rats may have reduced ability to properly suppress the oxidative stress due to its low function of antioxidant activity, resulting in damage of the brain.

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  • Development of a animal model of acute encephalopathy and an antibody therapy

    Grant number:26670500  2014.04 - 2017.03

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Challenging Exploratory Research

    Ohmori Iori

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    Grant amount:\3250000 ( Direct expense: \2500000 、 Indirect expense:\750000 )

    We tried to establish an animal model of acute encephalopathy with convulsive status epilepticus. We used Scn1a mutant rats because SCN1A mutations have been linked to hyperthermia-induced seizure susceptibility and acute encephalopathy with a prolonged seizure in human. We induced seizures with various conditions or by using drugs with a proinflammatory effect. Seizures are evoked in Scn1a mutant rats, however, they did not last more than 30 minutes which are often observed in acute encephalopathy in human. Various behavioral tests and pathological examinations of the brain were conducted after provoked seizures. They showed no cognitive impairment and motor disturbance. Pathological tests exhibited no brain edema nor inflammation.

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Class subject in charge

  • Seminar in Teaching Profession Practice (Elementary school) (2024academic year) 1st-4th semester  - 水7~8

  • Project Research in Educational Science (2024academic year) 1st-4th semester  - その他

  • Basic of Special Needs Education C (2024academic year) 1st semester  - 火5,火6

  • Basic of Special Needs Education A (2024academic year) 1st semester  - 月3~4

  • Basic of Special Needs Education A (2024academic year) 1st semester  - 火5~6

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