Analysis of the mechanism of Nfil3-mediated suppression of neurodegeneration
| Project/Area Number |
24700314
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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 |
Neuroscience in general
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| Research Institution | The University of Tokyo |
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Principal Investigator |
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 神経変性 / 筋萎縮性側索硬化症 / Nfil3 / 筋萎縮性側索硬化症（ALS） / 神経保護 / ALS |
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| Outline of Final Research Achievements |
Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by the loss of motor neurons. In this study, by using an ALS mouse model, we found that transcription factor Nfil3 is a neuroprotective molecule intrinsic to the neuronal defense mechanism. In addition, we searched for the molecule(s) which may acts downstream of Nfil3 and affects neuroprotective systems in cell-based ALS model. We identified a novel molecule which may constitute a cell defense mechanism in neurons.
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Report
(4 results)
Research Products
(11 results)
