Because ‘S1’ spike proteins support heparin and HBP interacions that promote the aggregation of Aβ peptides, α-synuclein, tau and prion proteins, SARS-CoV-2 infection itself may exacerbate the formation of amyloid peptide-enriched aggregates that support pro-inflammatory neurodegeneration, neuronal cell death and AD- and/or PrD-type change (Idrees and Kumar, 2021; Paiardi et al., 2022). The gene discussed is PRNP; the disease is Alzheimer disease.