Some clues about how the binding of Aβ to PrPC activates cPLA2 can be gathered from the prion literature, where aggregation of PrPC caused synapse damage in neurons similar to that seen with aggregates of PrPSc [19].The observations that Aβ oligomers that can cross-link PrPC are toxic, but Aβ monomers are not, indicate that the clustering of PrPC is key to cell signaling and link prion and Alzheimer’s diseases to a common pathway leading to neurodegeneration. The gene discussed is PRNP; the disease is early-onset autosomal dominant Alzheimer disease.