the immunopathogenic role of reactive oxygen species in alzheimer disease.

reactive oxygen species (ros) are produced in many normal and abnormal processes in humans, including atheroma, asthma, joint diseases, cancer, and aging. basal levels of ros production  in  cells  could  be  related  to  several  physiological functions  including  cell proliferation, apoptosis and homeostasis. however, excessive ros production above basal levels would impair and oxidize dna, lipids, sugars and proteins and consequently result in dysfunction of these molecules within cells and finally cell death. a leading theory of the cause of aging indicates that free radical damage and oxidative stress play a major role in the pathogenesis of alzheimer disease (ad). because the brain utilizes 20% more oxygen than other tissues that also undergo mitochondrial respiration, the potential for ros exposure increases. in fact, ad has been demonstrated to be highly associated with cellular oxidative stress, including augmentation of  protein  oxidation, protein  nitration, glycoloxidation and  lipid peroxidation as well as accumulation of amyloid β (aβ). the treatment with anti-oxidant compounds can provide protection against oxidative stress and aβ toxicity. in this review, our aim was to clarify the role of ros in pathogenesis of ad and will discuss therapeutic efficacy of some antioxidants studies in recent years in this disease.