Consistent with this conclusion, studies with a transgenic AD mouse model demonstrate48,49 increased levels of oxidative stress, AD pathology and enhanced cognitive dysfunction when double crossed with a knockout of antioxidant defences, including deficiencies in SOD50,51, and GPX52, while overexpression of SOD appears to reduce ROS levels, memory deficits and plaque load in respective AD mice48,49. This evidence concerns the gene SOD1 and Alzheimer disease.