| Project/Area Number |
17K10187
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Embryonic/Neonatal medicine
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| Research Institution | Nagoya City University |
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Principal Investigator |
KATO TAKENORI 名古屋市立大学, 医薬学総合研究院(医学), 研究員 (30381875)
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| Co-Investigator(Kenkyū-buntansha) |
齋藤 伸治 名古屋市立大学, 医薬学総合研究院(医学), 教授 (00281824)
神農 英雄 名古屋市立大学, 医薬学総合研究院(医学), 研究員 (40788387)
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| Project Period (FY) |
2017-04-01 – 2021-03-31
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| Project Status |
Completed (Fiscal Year 2020)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2019: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2018: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | 低酸素性虚血性脳症 / 内在性幹細胞 / 脳室下帯 / 内在性神経幹細胞 / 再生医学 / 脳・神経 |
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| Outline of Final Research Achievements |
In developing a new treatment for neonatal brain injury, we focused on neural stem cells in the subventricular zone of the brain. It is still unclear how neurogenesis in this region contributes to neuronal regeneration. In this study, we elucidated the molecular mechanisms that control the migration of neurons to the injured area in an animal model of neonatal brain injury, and evaluated whether transplantation of a migration scaffold based on this mechanism into the injured brain can promote neuronal regeneration. We also identified factors involved in neurogenesis at the molecular level by capturing gene expression changes in various cells in the subventricular zone during brain injury at the single-cell level, and developed basic technologies to identify new candidates for therapeutic drugs that promote neuro-regeneration.
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| Academic Significance and Societal Importance of the Research Achievements |
新生児低酸素性虚血性脳症は神経学的後遺症をもたらす周産期における重要な疾患である。現時点において科学的根拠を有した唯一の有効な治療法は脳低温療法であり、本疾患の予後改善のためには、新生児脳傷害の病態の解明と新たな機序による治療法の開発が必要である。本研究では脳室下帯とよばれる領域に存在する神経幹細胞に着目し、新生児脳障害モデル動物において脳障害時の内在性幹細胞の神経修復メカニズム、特に細胞の移動につき解析を行い、新たな治療法の可能性があることを示した。
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