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Elucidation of pathogenetic mechanism of amyotrophic lateral sclerosis caused by mutation in optineurin

Research Project

Project/Area Number 25860713
Research Category

Grant-in-Aid for Young Scientists (B)

Allocation TypeMulti-year Fund
Research Field Neurology
Research InstitutionHiroshima University

Principal Investigator

Kuramochi Masahito  広島大学, 原爆放射線医科学研究所, 特任助教 (30589122)

Project Period (FY) 2013-04-01 – 2016-03-31
Project Status Completed (Fiscal Year 2015)
Budget Amount *help
¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
Fiscal Year 2015: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2014: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2013: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Keywords筋萎縮性側索硬化症 / 神経変性 / オプチニューリン / 運動ニューロン / 脊髄 / SOD1 / 神経変性疾患
Outline of Final Research Achievements

Amyotrophic lateral sclerosis (ALS) is a progressive neurodegeneration disease of motor neurons resulting in the atrophy and weakness of muscle. Optineurin (OPTN) is one of genes causing ALS. It is thought that dysfunction and deletion of OPTN develop ALS. Therefore, I produced OPTN knockout mouse and then examined its mice behaviorally and histologically at both the young and the old age. At the results of these experiments, there was no significantly difference between non-genetically modified mice and the OPTN knockout mice. However, the deletion of OPTN prolonged survival in a transgenic mouse model of ALS.

Report

(4 results)
  • 2015 Annual Research Report   Final Research Report ( PDF )
  • 2014 Research-status Report
  • 2013 Research-status Report

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Published: 2014-07-25   Modified: 2019-07-29  

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