2017 Fiscal Year Final Research Report
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 |
Section | 一般 |
Research Field |
General pharmacology
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Research Institution | Tokyo Medical University |
Principal Investigator |
Nawa Mikiro 東京医科大学, 医学部, 講師 (10398620)
|
Project Period (FY) |
2015-04-01 – 2018-03-31
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Keywords | 筋萎縮性側索硬化症 / BTBD10 |
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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Free Research Field |
分子病態薬理学
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