| Project/Area Number |
17K16122
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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 | Osaka University |
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Principal Investigator |
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| Project Period (FY) |
2017-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2018: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2017: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | パーキンソン病 / alpha synuclein / 伝播 / エクソソーム / シヌクレイン / フィブリル / αシヌクレイン / パーキンソン |
|---|
| Outline of Final Research Achievements |
Endoplasmic reticulum-associated protein A was identified by analyzing the protein increased in exosomes when synuclein fibrils were highly expressed.
Overexpression of protein A increased the extracellular release of aSyn via exosomes. In addition, immunoprecipitation showed that αSyn was directly bound to protein A.Interestingly, when αSyn itself was overexpressed while protein A was overexpressed, αSyn-positive inclusion bodies were confirmed in the cells.
When comparing the amount of αSyn in exosomes when co-expressing protein A with fibril or monomer of αSyn pathogenic mutation, the G51D mutation was very strongly incorporated to exosome.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究では、αシヌクレインというパーキンソン病の発病原因の最も中核にある分子の一つが、どのように細胞から細胞に伝播していくか、その様式の一助を明らかにした。蛋白質Aの増加がパーキンソン病患者において特異的に、または加齢に伴い非特異的に、増加している場合、蛋白質Aの発現を押さえる治療がパーキンソン病の進展を予防する効果が期待できる。
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