Using different in vivo AD animal models, its effectiveness has been demonstrated in improving learning and memory deficits, due to its ability to relieve OS (↑CAT, SOD, and GSH), neuroinflammation (↓NF-kB), AChE activity, and tau phosphorylation, this latter event occurring via the modulation of the Akt/GSK-3β signaling pathway [312,313]. This evidence concerns the gene AKT1 and Alzheimer disease.