To determine if the presence of PrP amyloid promotes Aβ plaque generation “dual-disease” mice were generated by crossing Tg ceAPPswe/PS-1ΔE9 mice that model AD by co-expression of human APP with the Swedish mutation (APPswe) and presenilin-1 (PS-1) carrying the exon 9 deletion (hereafter referred to as TgAD mice) with Tg(PrP-A116V) mice (hereafter referred to as TgGSS mice) that express mouse sequence PrPA116V, a homolog of human PrPA117V that causes GSS22. The gene discussed is PRNP; the disease is Alzheimer disease.