| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2015: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2014: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2013: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Outline of Final Research Achievements |
Although the pathogenesis of prion disease has not been clarified fully, it is widely accepted that prion disease occurs through autocatalytic conformational conversion of the ubiquitous normal form of prion protein (PrPC) to PrPSc in a protein only manner. Meanwhile, activation of the innate immune system has been suggested to partially block the progression of prion disease. Furthermore, different prion strains can interfere with each other, and this is known as prion strain interference. The results suggest that cofactors, such as virus derived nucleic acids, involve in prion propagation. In this study, we demonstrated that double-stranded RNA innate immune responses play a key role in the pathogenesis of prion disease.
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