| Project/Area Number |
15K19486
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Neurology
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| Research Institution | Kyoto University |
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Principal Investigator |
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| Research Collaborator |
KINOSHITA Masato 京都大学, 大学院農学研究科, 助教
NAKANISHI Etsuro 京都大学, 大学院医学研究科, 大学院生
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2016: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | パーキンソン病 / ゴーシェ病 / 自然免疫 / メダカ |
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| Outline of Final Research Achievements |
GBA mutations are the strong risk factor of Parkinson’s disease. We have developed GBA－/－ medaka which display neuronal loss and alpha-synuclein accumulation accompanied with neuroinflammation. In this study, we analyzed the association of neuroinflammation with the pathophysiology in GBA－/－ medaka. MyD88 and TRIF are the adaptor molecules of TLRs. We successfully established MyD88 and TRIF knock-out medaka by CRISPR/Cas9. MyD88－/－ and TRIF－/－ medaka did not show any apparent abnormal phenotypes. Therefore, we analyzed GBA－/－MyD88－/－ and GBA－/－TRIF－/－ medaka, but any improvement in the neuronal loss or life span was not observed in those double mutant medaka compared to GBA－/－ medaka. These results suggest that signal pathways via MyD88 and TRIF do not associate with the pathophysiology in GBA－/－ medaka.
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