Prion protein in Alzheimer's pathogenesis: a hot and controversial issue.

The role for cellular prion protein PrP(c) in beta-amyloid (Abeta) oligomer-induced synaptic impairment is a topic of great interest and some controversy. In this issue of EMBO Molecular Medicine Aguzzi and co-workers explore the contribution of PrP(c) to deficient long term potentiation (LTP) and soluble Abeta levels in an Alzheimer's disease mouse model and show that the role of prions in Abeta related toxicity is far from 'black and white' suggesting complex interpretations of the data available thus far.