Stress and homeostatic regulation of oxidative damage in neurodegenerative disease

Recent evidence indicates that oxidative stress occurs early in the progression of Alzheimer disease, significantly before the development of the pathologic hallmarks, neurofibrillary tangles and senile plaques. Oxidative damage associated to Alzheimer disease elicits compensatory mechanisms that restore redox balance in an attempt to avoid neuronal death. We propose that oxidative modifications in Alzheimer disease may actually serve as a homeostatic response to stress resulting in a shift of neuronal priority from normal function to basic survival.