| Project/Area Number |
18K07363
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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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| Review Section |
Basic Section 51030:Pathophysiologic neuroscience-related
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| Research Institution | Chiba University (2019-2021)
Gunma University (2018) |
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Principal Investigator |
Naruse Masae 千葉大学, 大学院医学研究院, 特任講師 (60455219)
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| Project Period (FY) |
2018-04-01 – 2022-03-31
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| Project Status |
Completed (Fiscal Year 2021)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2020: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2019: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2018: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 神経幹細胞 / オリゴデンドロサイト / 脱髄 / ミクログリア / 髄鞘 / 髄鞘再生 / オリゴデンドロサイト前駆細胞 / 老化 |
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| Outline of Final Research Achievements |
When demyelination occurs, neural stem or progenitor cells in the SVZ provide newly formed oligodendrocytes to demyelinated lesions. The mechanisms, however, still remain unknown. The present study revealed that focal demyelination in the corpus callosum caused activation of microglia not only at the site of demyelination, but also in the SVZ, and dramatically increased generation of oligodendrocyte progenitor cells (OPCs) in the SVZ. Furthermore, inhibition of microglial activation decreased OPC generation in the SVZ, suggesting that activated microglia in the SVZ, induced by focal demyelination in the corpus callosum, regulate neural stem or progenitor cell lineage plasticity in situ. In contrast, inducing focal demyelination in the internal capsule did not induce either microglial activation or OPC generation in the SVZ. These results suggest that the mechanism of OPC generation in the SVZ following demyelinating lesions could be different among the demyelinated regions.
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| Academic Significance and Societal Importance of the Research Achievements |
内在性の神経幹細胞の活性化による髄鞘再生機構を明らかにする事は、難病である脱髄性疾患の再生医療の解明の発展へ貢献する。また、ミクログリアは脳内の免疫系を担う細胞であるが、近年、生理活性物質を放出して神経細胞やグリア細胞の生存や分化も制御している事が明らかになっている。本課題により、髄鞘再生におけるミクログリアの新しい役割と髄鞘再生過程における神経幹細胞の動態制御機構が明らかになった。
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