| Project/Area Number |
15K18367
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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 |
Nerve anatomy/Neuropathology
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| Research Institution | Yokohama City University |
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Principal Investigator |
TADA Mikiko 横浜市立大学, 附属病院, 助教 (30722467)
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| Research Collaborator |
DOI Hiroshi 横浜市立大学, 医学部, 准教授 (10326035)
KOYANO Shigeru 横浜市立大学, 医学部, 准教授 (50315818)
TANAKA Fumiaki 横浜市立大学, 医学研究科, 教授 (30378012)
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | matrin3 / ALS / polyglutamine / ポリグルタミン病 / FTLD / TDP43 / MATR3 / SALS |
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| Outline of Final Research Achievements |
Some of polyglutamine aggregate protein also has been shown to be a pathological gene or aggregation protein of amyotrophic lateral sclerosis(ALS)/frontotemporal lobar degeneration(FTLD). These facts indicated the possibility that shared pathway may exist in the degenerative process of polyglutamine diseases and ALS/FTLD. We aimed to identify novel ALS pathologically relevant molecules by pathological examination in autopsy tissue and to analysis of the pathological form and the characteristics of clinical course. We showed matrin 3 which is one of polygulutamine aggregate protein was a component of intracytoplasmic inclusion bodies in sporadic ALS. Additionally, mutation of MATR3 was reported as familial ALS responsible gene in 2015. Our results indicated that the broader involvement of matrin3 in ALS/FTLD and polyQ diseases.
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