期刊
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE
卷 1772, 期 6, 页码 598-609出版社
ELSEVIER
DOI: 10.1016/j.bbadis.2007.02.010
关键词
bovine spongiform encephalopathy; Creutzfeldt-Jakob disease; fatal familial insomnia; Gerstmann-Straussler-Scheinker disease; kuru; prion; prion disease; prion protein; transmissible spongiform encephalopathy; variant Creutzfeldt-Jakob disease
资金
- MRC [G0400713, MC_U123160655] Funding Source: UKRI
- Medical Research Council [G0400713, MC_U123192748, MC_U123160655] Funding Source: Medline
The recognition that variant Creutzfeldt-Jakob disease (vCJD) is caused by the same prion strain as bovine spongiform encephalopathy in cattle has dramatically highlighted the need for a precise understanding of the molecular biology of human prion diseases. Detailed clinical, pathological and molecular data from a large number of human prion disease patients indicate that phenotypic diversity in human prion disease relates in part to the propagation of disease-related PrP isoforms with distinct physicochemical properties. Incubation periods of prion infection in humans can exceed 50 years and therefore it will be some years before the extent of any human vCJD epidemic can be predicted with confidence. (c) 2007 Elsevier B.V. All rights reserved.
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