Herein, our aim is to investigate the detrimental effects of subacute and chronic Cd administration on accumulation of oxidative stress/ROS, Nrf2/HO-1, and activated p-JNK which might be associated with increased amyloid β (Aβ) level and hence possibly develop a feedforward mechanism which subsequently exacerbates AD pathologies in the aged mice’s brain. This evidence concerns the gene HMOX1 and Alzheimer disease.