In the classical view, in each disease of amyloid origin, one or two fibril-forming proteins were characterized, namely β-amyloid and tau proteins in Alzheimer’s disease, α-synuclein in Parkinson’s disease, huntingtin polyglutamine stretch in Huntington’s disease, prion protein in Creutzfeldt-Jakob disease and amylin in type II diabetes [7]. This evidence concerns the gene IAPP and early-onset autosomal dominant Alzheimer disease.