APP and Alzheimer disease: Multiple lines of evidence from biochemical, genetic and animal studies supports the theory that β-amyloid (Aβ) peptides of 40 and 42 residues, formed by enzymatic cleavage of amyloid precursor protein (APP), play a crucial role in the AD pathogenesis, where the aggregation of monomeric Aβ peptides to insoluble plaque-associated amyloid fibrils, such as annular protofibrills, cluster-like fibrils, etc. via soluble oligomeric intermediates, eventually lead to the neuronal cells death2–5.