2020 Fiscal Year Final Research Report
Neurodegeneration induced by ectopic mitochondrial DNA
| Project/Area Number |
18H02716
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Review Section |
Basic Section 51030:Pathophysiologic neuroscience-related
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| Research Institution | Niigata University |
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Principal Investigator |
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| Project Period (FY) |
2018-04-01 – 2021-03-31
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| Keywords | ミトコンドリアDNA / パーキンソン病 / リソソーム / IFI16 / DNaseII |
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| Outline of Final Research Achievements |
In this study, we showed that mitochondrial DNA leaks into the cytoplasm in cultured cells and zebrafish that mimic the state of Parkinson's disease. It was also shown that the inflammatory reaction and neurodegeneration are improved by inhibiting the sensor of mitochondrial DNA leaked into the cytoplasm and promoting the degradation of cytoplasmic mitochondrial DNA. In addition, mitochondrial DNA leaked into the cytoplasm and its sensor IFI16 were accumulated in PD brains. These results suggest that cytoplasmic leakage of mitochondrial DNA may be an important cause of neurodegeneration in Parkinson's disease.
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| Free Research Field |
病態神経科学、神経内科学
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| Academic Significance and Societal Importance of the Research Achievements |
これまでに見いだされていなかったパーキンソン病の新たな病態を明らかにした研究である。細胞質に漏出したミトコンドリアDNAの分解、あるいはそのミトコンドリアDNAセンサーの阻害が、パーキンソン病の病態に立脚した新規治療法につながる可能性がある。またパーキンソン病以外の疾患、例えば心不全や肝臓線維化などでも同様のメカニズムが存在する可能性がある。パーキンソン病のさらなる解明や治療の開発と並行して、その他の疾患解析も検証を進める。
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