| Project/Area Number |
23300204
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Rehabilitation science/Welfare engineering
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| Research Institution | National Rehabilitation Center for Persons with Disabilities |
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Principal Investigator |
OGATA Toru 国立障害者リハビリテーションセンター(研究所), 研究所 運動機能系障害研究部, 研究部長 (00392192)
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| Co-Investigator(Kenkyū-buntansha) |
SUGIMORI Michiya 富山大学, 大学院・医学薬学研究部(医学), 助教 (20464026)
森岡 和仁 国立障害者リハビリテーションセンター(研究所), 研究所・運動機能系障害研究部, 流動研究員 (90551466)
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| Project Period (FY) |
2011-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥15,860,000 (Direct Cost: ¥12,200,000、Indirect Cost: ¥3,660,000)
Fiscal Year 2013: ¥3,380,000 (Direct Cost: ¥2,600,000、Indirect Cost: ¥780,000)
Fiscal Year 2012: ¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2011: ¥8,450,000 (Direct Cost: ¥6,500,000、Indirect Cost: ¥1,950,000)
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| Keywords | オリゴデンドロサイト / 協調運動 / 細胞培養 / 痙縮 |
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| Research Abstract |
In this study, we examined the mechanisms of remyelination, which is one of therapeutic targets in spinal cord injury. We found that maturation of oligodendrocytes, myelin forming cells in spinal cord, is negatively regulated by Ascl1-Hes5 axis in developmental stage, but the progenitors in adult spinal cord do not express Hes5, indicating they are relatively mature progenitors. Suppression of remaylination in mouse spinal cord injury model leads to deficit in motor function recovery, which indicates the importance of remyelination processes. Taken together, to establish therapeutic approach to remyelination, we should consider the mechanisms governing oligodendrocyte functions.
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