To date, this detrimental interaction with PrP has been shown for oligomers of Amyloid-β (Aβ), tau, and α-synuclein, which are critically associated with Alzheimer’s disease (AD), frontotemporal dementia and other tauopathies, or Parkinson’s disease, respectively (Corbett et al. 2020; Ferreira et al. 2017; Hu et al. 2018; Ondrejcak et al. 2018). This evidence concerns the gene PRNP and early-onset autosomal dominant Alzheimer disease.