Alternatively, injected fibrillated α-synuclein into transgenic mice models of AD were unsuccessful at cross-seeding Aβ in vivo, and the mice that co-expressed the A30P mutations of α-synuclein appeared to inhibit the formation of plaques in the mutant amyloid precursor protein (APP), as well as presenilin 1 [209]. The gene discussed is APP; the disease is Alzheimer disease.