| Project/Area Number |
15K09342
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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 |
Neurology
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| Research Institution | Kyushu University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
山崎 亮 九州大学, 医学研究院, 准教授 (10467946)
真崎 勝久 九州大学, 医学研究院, 助教 (90612903)
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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 |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2017: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2016: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2015: ¥3,120,000 (Direct Cost: ¥2,400,000、Indirect Cost: ¥720,000)
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| Keywords | 筋萎縮性側索硬化症 / 変異SOD1トランスジェニックマウス / マクロファージ / ミクログリア / CCR2 / 末梢神経 / M2 |
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| Outline of Final Research Achievements |
We analyzed the influence of monocyte migration inhibition on the pathology of ALS model mice by mating ALS model mice (mSOD1 mice) and MCP-1 receptor deficient mice (CCR2 - / - mice). As a result, CCR2 - / - mSOD1 mice developed initial sign of hind-limb weakness earlier than conventional mSOD1 mice. Conventional mSOD1 mouse had inflammatory cell infiltration into the peripheral nerve before disease onset. These inflammatory cells phagocytosed the mutant SOD1 protein. Inflammatory cell infiltration into the peripheral nerve were markedly suppressed in CCR2 - / - mSOD1 mice. Since promotion of disease progression was observed despite weak inflammatory cell infiltration into the peripheral nerve in CCR2-/-mSOD1 mice, it was strongly suggested that these inflammatory cells may act neuroprotectively.
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