As previously suggested by a study in brains of patients suffering from Alzheimer’s disease, this discrepancy has two possible explanations: first, the excess of SOD enzyme that is synthesized under conditions of high oxidative stress may be subsequently inactivated; second, the SOD enzyme could be concentrated in the site of increased oxidative stress, despite an overall reduction in its activity (Omar et al., 1999). This evidence concerns the gene SOD1 and Alzheimer disease.