Furthermore, Esposito and colleagues have shown that in human amyloid precursor protein (hAPP) transgenic mice, inactivating one Sod2 allele (Sod2+/−) and reducing Sod2 activity exacerbates Alzheimer’s disease-like pathology and have suggested that increasing Sod2 activity might be of therapeutic benefit whereas Clausen and colleagues have explicitly demonstrated prevention of cognitive deficits and brain oxidative stress with superoxide dismutase/catalase mimetics in aged mice [157,158]. Here, SOD2 is linked to early-onset autosomal dominant Alzheimer disease.