Knockout of SOD2 increased amyloid plaque burden and exacerbated cognitive deficits in mice (Li et al., 2004; Esposito et al., 2006; Lee et al., 2012), and conversely, SOD2 overexpression reduced oxidative markers, amyloid deposition, and cognitive deficit in transgenic AD mice (Dumont et al., 2009). The gene discussed is SOD2; the disease is Alzheimer disease.