BACE1 and Alzheimer disease: In addition to the classic Aβ peptides generated from the precursor protein APP by the combined activity of BACE1 and γ-secretase—starting at the aspartate residue at position 1 and ending at amino acids 38/40/42—multiple truncated Aβ species exhibiting different solubility properties have been identified in cellular and animal models as well as in AD patients [11, 30–40].