. Cellular prion protein mediates impairment of synaptic plasticity by amyloid-beta oligomers. Nature. 2009 Feb 26;457(7233):1128-32. PubMed.

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  1. This paper reports the surprising identification by expression cloning of the prion protein (PrP) as a receptor for Aβ oligomers and the synaptotoxic consequences of this interaction. There is extensive evidence in support of these findings, and if confirmed by other labs, PrP could be an important new target for AD therapeutics...so long as such compounds do not induce PrP into an aggregation-prone form called PrPsc, which causes devastating spongiform encephalopathies (e.g., CJD in humans). That would be a side effect that would be worse than the disease that one is trying to treat!