| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2012: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2011: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Research Abstract |
Prion diseases are infectious and fatal neurodegenerative disorders characterized by progressive spongiform changes and the accumulation of abnormal prion protein (PrPSc) in the central nervous system. Although prion diseases were thought to be caused by slow-virus infections, no exogenous viral genome has been identified. The infectious agent, now called prion, is thought not to possess its own genome and to be composed uniquely of prion proteins, which are encoded by the host gene. In this study, we found that polyinosine-polycytidylic acid (poly(I:C)), a synthetic analog of dsRNA,-treated mice increased accumulation of PrPScin prion-infected cells, and accelerated the onset of prion disease in wild-type mice. Moreover, PrPScwas increased by overexpression of Toll-like receptor 3 (TLR3), Retinoic acid-inducible gene-I (RIG-I), and Melanoma differentiation-associated protein 5 (MDA5), which recognize dsRNA, in prion-infected cells. Our findings suggest that dsRNA may play a key role in prion infection.
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