Besides acting as an antioxidant activator of mitochondrial aconitase, one of the enzymes of the citric acid cycle that is affected by the oxidative stress in AD [179], melatonin was reported to act as a defensive agent against Aβ-induced cytotoxicity in BV2 microglial cells; it attenuated the cellular apoptosis by activating Bcl-2 antiapoptotic pathways, thus involving higher Bcl-2 expression and reduced Bax mRNA level and caspase-3 activity [197]. This evidence concerns the gene BAX and Alzheimer disease.