The role of oxidative damage in the pathogenesis of AD is reflected by altered activity of antioxidant enzymes (SOD, catalase) and increased levels of OS biomarkers (malondialdehyde, 4-hydroxynonenal, and F2-isoprostane protein are markers of lipid oxidative damage; protein carbonyls and 3-nitrotyrosine are products of protein oxidation, whereas 8-hydroxydeoxyguanosine reflects nucleic acid oxidation) in the blood and cerebrospinal fluid of patients with AD [11, 52, 53]. The gene discussed is SOD1; the disease is Alzheimer disease.