For instance, the activities of SOD, CAT and GPX have been described to be significantly low in early AD [190,191]; in particular, SOD activity seems to be significantly reduced in both the extracellular and intracellular blood compartments [192,193], and SOD deficiency has been related to the increased deposition of Aβ and memory impairments, both alleviated by SOD-2 overexpression [194]. The gene discussed is SOD1; the disease is Alzheimer disease.