Multiple labs additionally described two Aβ binding sites present on PrPC, identified signalling pathways activated by the interaction, and demonstrated that PrPC ablation, or inhibition mediated by anti-PrPC antibodies, prevents Aβ associated synaptotoxicity in vitro and in vivo, providing therapeutic proof of principle [5–11] such that PrPC is now a recognised and validated receptor for Aβ in the AD field. This evidence concerns the gene PRNP and Alzheimer disease.