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2017 Fiscal Year Final Research Report

Relationship between reduction of BTBD10 expression in motor neuron and pathogenesis and progression of amyotrophic lateral sclerosis.

Research Project

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Project/Area Number 15K08245
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field General pharmacology
Research InstitutionTokyo 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
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.

Free Research Field

分子病態薬理学

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Published: 2019-03-29  

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