In addition, myricetin administration has been shown to reverse D-galactose-induced decreases in SOD activity and increases in levels of thiobarbituric acid reactive substances (TBARS) (Lei et al., 2012; Figure 3 and Table 2), or scopolamine-induced increases in malondialdehyde (MDA) levels and decreases in SOD, glutathione peroxidase (GPx), and catalase activities in the hippocampus (Wang et al., 2017; Figure 3 and Table 2), suggesting that anti-oxidation may mediate the anti-AD’s effects of myricetin, at least in rodent models of D-galactose or scopolamine stimulation. Here, SOD1 is linked to Alzheimer disease.