Regulation of the following mitochondrial functions by small molecules appears promising in AD treatment: protein acetylation (which is regulated by coenzyme NAD+, tricarboxylic acid cycle activity, OXPHOS, sirtuins, and nicotinamide phosphoribosyl transferase), inhibition of the mitochondrial calcium uniporter, inhibition of mPTP opening, and modulation of mitochondrial morphology and dynamics (by the outer mitochondrial membrane fusion protein mitofusin, the inner membrane fusion protein dynamin-like 120 kDa, and the fission protein DRP1) [30,224,326]. This evidence concerns the gene DNM1L and Alzheimer disease.