Freir et al. demonstrated that PrPC is a major component for the inhibition of LTP by ADDLs from AD brains, which is consistent with research showing that oligomeric Aβ assemblies bind with strong specificity to PrPC to trigger the disruption of synaptic plasticity in vitro and in vivo (Freir et al., 2011; Kostylev et al., 2015). The gene discussed is PRNP; the disease is Alzheimer disease.