2016 Fiscal Year Final Research Report
Development of pathological mechanism and therapy for amyotrophic lateral sclerosis using optineurin mice
| Project/Area Number |
26293211
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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 |
Neurology
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| Research Institution | Hiroshima University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
川上 秀史 広島大学, 原爆放射線医科学研究所, 教授 (70253060)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Keywords | 筋萎縮性側索硬化症 / オプチニューリン / ノックアウトマウス |
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| Outline of Final Research Achievements |
We generated optineurin (OPTN) knockout (KO) mice. Compared to wild-type mice, 24-month-old OPTN-KO mice did not differ for survival curve, body weight or motor function. Inclusion body like structures were observed in the cell bodies of motor neurons in the lumbar spinal cord. Golgi fragmentation was increased. Axonal degeneration was observed in sciatic nerve.
Double modification mice of SOD1 and OPTN showed elongation of life time.
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| Free Research Field |
神経内科
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