ACHE and Alzheimer disease: Thus, various approved acetylcholinesterase drugs have been repositioned for further derivatizations, by enclosing or fusing other molecular entities to interact with some other AD targets, namely those related with the toxic amyloid plaque, such as the inhibition of β-amyloid (Aβ) fibril formation (e.g., inhibition β-Secretase, BACE-1) and its aggregation, as well as the control of effects of oxidative stress and metal dyshomeostasis, due to their recognized role in deleterious protein/peptide modification and aggregation [9,10,11,12].