In oligomeric amyloid-β25–35 peptide (Aβ25–35)-injected mouse model of AD, it was observed that administration of Sig-1R agonists ANAVEX2-73 and PRE-084 not only inhibited Aβ25–35-induced elevation of lipid peroxidation levels and Bax/Bcl-2 ratio, as well as release of cytochrome c, all of which are related to mitochondrial integrity, but also corrected Aβ25–35-induced mitochondrial respiratory dysfunction and aberrant increase of reactive oxygen species (ROS) and apoptosis (Lahmy et al., 2014). This evidence concerns the gene BAX and Alzheimer disease.