Explore a novel mechanism for neurodegenerative disease using Caspr deficient mutant mice
Project/Area Number |
23591241
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Neurology
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Research Institution | Nagoya University |
Principal Investigator |
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Research Collaborator |
KATANOSAKA Kimiaki 中部大学, 生命健康科学部・生命医科学科, 准教授
MIZOGUCHI Hiroyuki 名古屋大学, 環境医学研究所・次世代創薬研究センター, 助教
|
Project Period (FY) |
2011-04-28 – 2015-03-31
|
Project Status |
Completed (Fiscal Year 2014)
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Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2013: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2011: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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Keywords | 神経変性疾患 / ランビエ絞輪 / パラノード / 遺伝性疾患マウス / 神経筋伝達 / 神経変性 / 興奮伝導 / 骨格筋 / 有髄神経線維 / 神経軸索変性 / 神経細胞死 / ランビエの絞輪 / 軸索変性 / ミュータントマウス / 軸索骨格 / ニューロフィラメント |
Outline of Final Research Achievements |
We identified a mutation of the Caspr gene in a mouse mutant shambling (shm). We analyzed dysfunction of the paranode at nodes of Ranvier and impaired nerve conduction in myelinated nerves of shm mice. The shm mice manifest the progressive neurological defect as mice age. We studied a pathophysiological process of the disease in the nervous system of shm mice and found that axons and neurons were severely damaged and resultant loss of neurons occurred in various regions of the nervous system in aged mice but not in young or adult mice. This study is a first demonstration of neuron death in the nervous system among the paranodal mutants. Further in this study we identified various parallelisms between shm mice and human neurodegenerative disease. We would like to propose that our study provides a novel prospect in a study to explore a mechanism of human neurodegenerative disease.
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Report
(5 results)
Research Products
(6 results)