2014 Fiscal Year Final Research Report
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 |
Research Field |
Neuroscience in general
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Research Institution | The University of Tokyo |
Principal Investigator |
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Project Period (FY) |
2012-04-01 – 2015-03-31
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Keywords | 神経変性 / 筋萎縮性側索硬化症 / Nfil3 |
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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Free Research Field |
発生神経科学
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