2015 Fiscal Year Final Research Report
Elucidation of pathogenetic mechanism of amyotrophic lateral sclerosis caused by mutation in optineurin
| Project/Area Number |
25860713
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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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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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Keywords | 筋萎縮性側索硬化症 / 神経変性 / オプチニューリン / 運動ニューロン / 脊髄 / SOD1 |
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| Outline of Final Research Achievements |
Amyotrophic lateral sclerosis (ALS) is a progressive neurodegeneration disease of motor neurons resulting in the atrophy and weakness of muscle. Optineurin (OPTN) is one of genes causing ALS. It is thought that dysfunction and deletion of OPTN develop ALS. Therefore, I produced OPTN knockout mouse and then examined its mice behaviorally and histologically at both the young and the old age. At the results of these experiments, there was no significantly difference between non-genetically modified mice and the OPTN knockout mice. However, the deletion of OPTN prolonged survival in a transgenic mouse model of ALS.
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| Free Research Field |
神経科学
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