Amyloid-beta, a protein well known for its role in Alzheimer's disease, may yield its damaging effects on neurons by binding to the cellular prion protein (PrPC), a paper published in Nature suggests. This could make PrPC a potential target for Alzheimer's disease therapeutics.
Misfolded variants of PrPC have been implicated in prion diseases, such as bovine spongiform encephalopathy (BSE), but the normal endogenous version is found in many types of cell. In neurons, PrPC appears to act as a receptor for the amyloid-beta protein, Stephen Strittmatter and colleagues report. Moreover, they show that the deleterious effects of amyloid-beta on long-term potentiation in brain slices, an experimental model for learning and memory, are mediated by PrPC.
Stephen Strittmatter (Yale University School of Medicine, New Haven, CT, USA)
(C) Nature press release.
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