APP and Alzheimer disease type 1: These proteinaceous deposits form as a consequence of the aggregation of the intrinsically disordered amyloid-β peptide (Aβ), a proteolytically derived transmembrane fragment of the amyloid precursor protein (APP), and a multitude of biochemical, genetic and animal investigations point to the aberrant behaviour of this molecule as central to the aetiology of AD1–5,7.