| Project/Area Number |
23780303
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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 |
Applied veterinary science
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| Research Institution | Hokkaido University |
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Principal Investigator |
HASEBE RIE 北海道大学, (連合)獣医学研究科, 講師 (70431335)
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| Project Period (FY) |
2011 – 2012
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2012: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2011: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | プリオン病 / 補体因子 / 補体 / 初代培養神経細胞 / 神経変性 |
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| Research Abstract |
Although complement factors have been detected in brains of patients and animals affected by prion diseases, the roles in the pathogenesis still remain unknown. In the current study, reaction of complement factors increased permeability of the plasma membrane of primary-cultured neurons infected with prions, but not cell death. This phenomenon was observed in the neurons infected with either Chandler or 22L strains, however, the effect on propagation of an abnormal form of prion protein (PrPSc) was opposite: inhibition in the Chandler-infected neurons, and acceleration in the 22L-infected neurons. The results of this study would be expanded to the other prion strains in the future, to assess a possibility that regulation of complement pathway could be a therapeutic target of prion diseases.
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