Relationship between reduction of BTBD10 expression in motor neuron and pathogenesis and progression of amyotrophic lateral sclerosis.
| Project/Area Number |
15K08245
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
General pharmacology
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| Research Institution | Tokyo Medical University |
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Principal Investigator |
Nawa Mikiro 東京医科大学, 医学部, 講師 (10398620)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 筋萎縮性側索硬化症 / BTBD10 |
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| Outline of Final Research Achievements |
We previously reported that the expression level of BTBD10 was reduced in motor neuron of amyotrophic lateral sclerosis (ALS) patient. In this study, we generated BTBD10 transgenic (-Tg) mouse and knockout (-KO) mouse to research the relationship between reduction of BTBD10 expression in motor neuron and ALS pathogenesis and disease progression.
First, we mated BTBD10-Tg mouse and G93A-SOD1-Tg mouse, an ALS model mouse, to observe the effect of expression of BTBD10 on progression of ALS pathology. The onset and the life span of double-Tg mouse were almost same as G93A-SOD1-Tg mouse. Next, we generated BTBD10-KO mouse and observed motor function with rotarod test. The latency to fall from a rotating rod of the 6-month-old BTBD10-KO mouse tend to be shorter than that of wild type mouse.
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Report
(4 results)
Research Products
(4 results)
