| Project/Area Number |
25870479
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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
Veterinary medical science
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| Research Institution | The University of Tokushima |
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Principal Investigator |
HARA Hideyuki 徳島大学, 疾患酵素学研究センター, 助教 (40469953)
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2013: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | プリオン / 構造変換 / 銅イオン / オクタペプチドリピート / OR / リピート部位 / 銅 / 神経変性 / クロイツフェルト・ヤコブ病 / 狂牛病 / スクレイピー |
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| Outline of Final Research Achievements |
Prion diseases are characterized by the replicative propagation of disease-associated forms of prion protein (PrPSc; PrP refers to prion protein). Structural conversion of the normal cellular isoform, designated PrPC, into PrPSc is a key event in prion propagation. However, the conversion mechanism remains unclear. In this study, we intracerebrally inoculated prions into tg(PrPΔOR)/Prnp0/0 mice, which express mouse PrP missing only the octapeptide repeat (OR) region on the PrP-null background. There are different incubation time in infected the prions. As a result, the mechanism of structural conversion was depending on the type of prions. Also we examined the effects of copper ions on the pathological progression of prion disease. However, copper ions didn't have any influence on the pathological progression.
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