In this respect, given the pivotal roles played by the cellular prion protein (PrPC) as a high-affinity neuronal receptor for Aβ oligomers and in neurotoxic Aβ oligomer-induced synaptic dysfunction in AD [8], a comparative study on brain PrPC expression in cetaceans with AD-like alterations could provide valuable information on the pathogenetic links of their encephalopathy, if any, with human AD [9]. The gene discussed is PRNP; the disease is Alzheimer disease.