PRNP and Alzheimer disease: The neurotoxic soluble Aβ oligomers, including the most toxic oligomeric Aβ42, have been shown to alter synaptic plasticity and synaptic transmission in various AD animal models via a variety of synaptic targets of Aβ such as ionic neurotransmitter receptors, G protein-coupled receptors (GPCRs), receptor tyrosine kinases, and cellular prion proteins (PrPC)9,10.