At present, in different animal AD models as well as in patients with AD, it has been established that PrPC could be one of the best specific binding partners for AβOs-mediated inhibition of LTP and cognitive defects in the early stages of AD (Kostylev et al., 2015; Smith and Strittmatter, 2017; Smith et al., 2019; Corbett et al., 2020). The gene discussed is PRNP; the disease is Alzheimer disease.