The oxidative stress state may mediate the deposition of Aβ, associated with mitochondrial damage and reduced synaptic plasticity, which is consistent with the results of the present study, in which ROS, H2O2, and MDA levels were significantly increased in the AD brain, with ROS often thought to mediate mitochondrial damage associated with AD brain and MDA mediating lipid peroxidation in AD brain, while EX or GCA reversed this phenomenon and increased CAT. This evidence concerns the gene CAT and Alzheimer disease.