BACE1 and Alzheimer disease: The molecular structures of 2c and 5c could also be further modified and synthesized as prodrugs to enhance and extend their capacities to treat AD beyond their structural breakdown, as a result of drug metabolism, which may produce active metabolites such as ascorbic acid (a potent amyloid aggregation inhibitor and antioxidant and anti-inflammatory agent) and tryptoline (BACE1, ChE, and MAO inhibitors [21,22,23]).