BACE1 and Alzheimer disease: New hybrids were designed by linking two privileged chemotypes with well-known therapeutic activities in AD and other NDs: (i) a flavonoid core derived from 4-chromenone or 4-quinolone, with potential neurogenic properties38 and inhibition of BACE-139, LOX-540 and MAO41; and (ii) the N,N-dibenzyl(N-methyl)amine (DBMA) fragment, present in AP223842–44 and other AD-directed MTDLs45,46, due to its proved interaction with the catalytic anionic site (CAS) of AChE47 (Figure 1).