Following identification of PrPC as a high affinity receptor for AβO (43), immuno-targeting of PrPC was shown to block completely the LTP impairments caused by AβO derived from human AD brain extracts (70, 71), and intra-cerebral infusion of an anti-PrPC monoclonal antibody reversed the memory impairments in a transgenic AD mouse model (72). The gene discussed is ABO; the disease is Alzheimer disease.