Therefore, secondary metabolites from natural sources that inhibit GSK-3β could be a promising strategy for AD treatment and, as recently reported, inhibition of GSK-3 can be achieved by N-terminal serine phosphorylation on GSK-3α (serine-21/S21) and GSK-3β (serine-9/S9), targets kinases such as protein kinase A and protein kinase B (PKB/AKT), and prevents GSK-3 binding to its substrates [23]. This evidence concerns the gene AKT1 and Alzheimer disease.