Aβ-induced tau hyperphosphorylation is processed through the activation of glycogen synthase kinase-3 beta (GSK-3β), MAPKs, hyperhomocysteinemia (HHcy), and cyclin-dependent kinase 5 (CDK5); the balance between GSK-3β and protein phosphatase 2A (PP2A) activities determines the phosphorylation status of tau in an AD brain [13,17,61]. This evidence concerns the gene GSK3B and hyperhomocysteinemia.