Investigation of the role of neuronal cell deth in a neurodegenerative prosess of ALS model mice
| Project/Area Number |
25870754
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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
Neurochemistry/Neuropharmacology
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| Research Institution | Jikei University School of Medicine |
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Principal Investigator |
Hara Chikako 東京慈恵会医科大学, 医学部, 助教 (40528452)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2015: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 筋萎縮性側索硬化症 / 前頭側頭変性症 / ALS / FTLD / 細胞内凝集体 / 神経変性 / 神経変性疾患 / 細胞内凝集体形成 / モデルマウス / 筋委縮性側索硬化症 |
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| Outline of Final Research Achievements |
We had planed to investigate the abnormal cytoplasmic inclution and neuronal cell deth caused by TAR DNA Binding Protein-43(TDP-43) of ALS model mice. TDP-43 has been identified as a causative gene of both amyotrophic lateral scleosis(ALS) and frontotemporal lober degeneratiion (FTLD), based on the findings that cytoplasmic inclusion bodies in ALS and FTLD pathology.
Details of cytoplasmic inclusion forming processes were investigated by this study. Specificaly, the abnormal flagmentation of TDP-43 protein in cultured cells, the frequency of the abnormal cytoplasmic inclusions, and decrease in number of the spinal cord neuron of the adult ALS model mice were detected.
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Report
(4 results)
Research Products
(5 results)
