Specifically, studies have indicated that oxidative stress might play a major role in AD pathogenesis [86], due to direct evidence of increased neurotoxic markers of lipid peroxidation, such as 4-hydroxynonenal, in human subjects [87], excessive brain protein oxidation in AD [88], increased nuclear DNA oxidation in the brain of AD patients [89], 30% increased activity of the free radical scavenging enzyme SOD-1 in cell lines of AD patients [90], and significantly, direct evidence that beta amyloid generates free radical peptides [70, 91]. The gene discussed is SOD1; the disease is Alzheimer disease.