Past and Future of Diagnosis and Therapy of Transmissible Spongiform Encephalopathy
作者： Chih-Yuan Tseng , Jack Tuszynski
DOI: 10.5772/28998
关键词: Scrapie 、 Proteinase K 、 Prion protein 、 Biology 、 Bovine spongiform encephalopathy 、 Transmissible spongiform encephalopathy 、 Amyloid fibril 、 Virology
摘要: Transmissible spongiform encephalopathies (TSEs), also known as prion diseases, including Creutzfeldt-Jakob disease (CJD) in human, Bovine Spongiform Encephalopathy (BSE) cow, and scrapie sheep, represent diseases with complex still poorly understood molecular mechanisms (Prusiner, 1998). The protein-only hypothesis postulates a possible pathogenic mechanism involving the protein. helix rich normal protein (PrPC) is found to be infected by its -sheet abnormal proteinase K (PK)-resistant form, PrPSc, converted into PrPSc This infection will lead aggregation of PrPSc-based amyloid fibrils that accumulate peripheral invade central nervous system damage neurons.
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