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). The gene discussed is SOD1; the disease is early-onset autosomal dominant Alzheimer disease.