期刊
SCIENCE
卷 302, 期 5646, 页码 871-874出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1090187
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资金
- Medical Research Council [MC_U132692719, MC_U123160654] Funding Source: Medline
- Medical Research Council [MC_U123160654] Funding Source: researchfish
- MRC [MC_U123160654] Funding Source: UKRI
The mechanisms involved in prion neurotoxicity are unclear, and therapies preventing accumulation of PrPSc, the disease-associated form of prion protein (PrP), do not significantly prolong survival in mice with central nervous system prion infection. We found that depleting endogenous neuronal PrPc in mice with established neuroinvasive prion infection reversed early spongiform change and prevented neuronal loss and progression to clinical disease. This occurred despite the accumulation of extraneuronal PrPSc to levels seen in terminally ill wild-type animals. Thus, the propagation of non-neuronal PrPSc is not pathogenic, but arresting the continued conversion of PrPc to PrPSc within neurons during scrapie infection prevents prion neurotoxicity.
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