Compelling evidence supports the importance of metabolic abnormalities in Alzheimer disease pathogenesis. Indeed, that oxidative mechanisms are involved in the neuropathology associated with Alzheimer disease is evidenced by the large number of metabolic signs of oxidative stress as well as by specific markers of oxidative damage. However, in the initial stages of disease development, neurons adapt to the oxidative environment through the development of compensatory responses resulting in a shift of neuronal priority from normal function to basic survival.