Journal
SCIENCE
Volume 303, Issue 5663, Pages 1514-1516Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1094273
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Funding
- NHLBI NIH HHS [HL63817] Funding Source: Medline
- NIAID NIH HHS [AI09484] Funding Source: Medline
- NIA NIH HHS [AG04342, AG00080] Funding Source: Medline
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Neuronal death is a prominent, but poorly understood, pathological hallmark of prion disease. Notably, in the absence of the cellular prion protein (PrPC), the disease-associated isoform, PrPSc, appears not to be intrinsically neurotoxic, suggesting that PrPC itself may participate directly in the prion neurodegenerative cascade. Here, cross-linking PrPC in vivo with specific monoclonal antibodies was found to trigger rapid and extensive apoptosis in hippocampal and cerebellar neurons. These findings suggest that PrPC functions in the control of neuronal survival and provides a model to explore whether cross-linking of PrPC by oligomeric PrPSc can promote neuronal loss during prion infection.
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