| Project/Area Number |
25282166
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Partial 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 | Fujita Health University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
林 宣宏 東京工業大学, 生命理工学研究科, 准教授 (80267955)
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| Co-Investigator(Renkei-kenkyūsha) |
SINZATO MASANORI 藤田保健衛生大学, 医療科学部, 准教授 (80148288)
INAGAKI HIDETO 藤田保健衛生大学, 総合医科学研究所, 講師 (70308849)
CHIHARA TAKESHI 藤田保健衛生大学, 藤田記七栗研究所, 准教授 (00217241)
MIZUTANI KENMEI 藤田保健衛生大学, 藤田記七栗研究所, 講師 (30351068)
SHIMPO HIROSHI 藤田保健衛生大学, 藤田記七栗研究所, 講師 (10142580)
SONODA SHIGERU 藤田保健衛生大学, 医学部, 教授 (10197022)
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| Project Period (FY) |
2013-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥17,030,000 (Direct Cost: ¥13,100,000、Indirect Cost: ¥3,930,000)
Fiscal Year 2016: ¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
Fiscal Year 2015: ¥3,120,000 (Direct Cost: ¥2,400,000、Indirect Cost: ¥720,000)
Fiscal Year 2014: ¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2013: ¥5,980,000 (Direct Cost: ¥4,600,000、Indirect Cost: ¥1,380,000)
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| Keywords | 小脳失調症 / リハ運動訓練 / プルキンエ細胞変性 / 運動失調 / 歩行解析 / 環境エンリッチメント飼育 / 原因遺伝子解析 / 染色体構造異常 / 小脳変性マウス / 運動失調症 / 次世代シークエンサー解析 / 神経シナプス / 神経栄養 / D型セリン / 強制運動負荷 / 小脳失調 / リハビリ訓練 / 原因遺伝子 / アンキリンＧ / ＮＧＳエクソーム解析 / メイトペアライブラリ / セリン / シナプス受容体 / 小脳性運動失調 / 遊離アミノ酸 / マウス用歩行解析 / マウス用重心動揺 / 遺伝子産物検索 / 脳卒中回復期リハビリ / 神経変性 / 生体成分 / 微量検体分析 / 質量分析 / 遺伝子産物 / UPLC |
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| Outline of Final Research Achievements |
We applied different rehabilitation methods which are known to be effective in reducing ataxia to cerebellar ataxic B6-Wob/tmice and examined those methods in terms of nature and load. The effect of training was evaluated by applying forced walk training. Furthermore, the effect of voluntary walk training in an environmental enriched mouse cage was also evaluated.The observations of cooperative walk training, brain weight, Purkinje cell degeneration were used for evaluation.We could verify the importance of the effect of forced walk training regardless of the strength and the load of training.Although we were in search of the gene that causes the degeneration of cerebellar, we found structural chromosome abnormalities in the 10th chromosome.Currently, we are investigating the similarity of our findings with the gene that causes spinocerebellar ataxia onset in patients.
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