| Project/Area Number |
23500590
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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 |
Rehabilitation science/Welfare engineering
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| Research Institution | Kagoshima University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
YOSHIDA Yoshihiro 鹿児島大学, 名誉教授 (10107906)
MATSUDA Fumiyo 鹿児島大学, 医学部, 助教 (70437953)
IJIRI Kosei 鹿児島大学, 医歯研, 客員研究員 (00315417)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2013: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2011: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | リハビリテーション / 脳神経保護作用 / 運動療法 / 神経栄養因子 / 脳神経保護 / 機能回復促進 / 早期運動療法 / ロボットスーツHAL / 脳梗塞 / 神経保護 / メカニズム |
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| Research Abstract |
We examined whether exercise reduces brain infractions, decreases neuronal apoptotic cell death, and improves neurobehavioral functions via the PI3K/Akt dependentpathway using rat middle cerebral artery occlusion (MCAO) model.Motor exercise provided neuroprotection, reduced neuronal cell death, maintained tissue structure, and aided functional recovery by stimulating the expression of neurorepair mediators BDNF/pTrkB via activating Akt2). Because the benefit of exercise in neurorepair hasbeen linked with the activation of the PI3 kinase/Akt pathway, we used aselective PI3 kinase inhibitor LY to confirm this mechanism in our study.
Exercise improved neurobehavioral functions, indicating that the reduced deficits are related with the exercise-mediated decreased neuronal apoptotic cell death. Early motor exercise aid functional recovery by stimulating neurorepair mechanisms after stroke.
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