The literature data of animals suggest that the BPA-induced disruption of insulin signaling may be involved in induced AD-like neurotoxicity through the signaling pathway mediated by Akt and phosphatidylinositol 3-kinase (PI3K)-dependent mechanisms, resulting in the phosphorylation of Akt and activation of glycogen synthase kinase 3β (GSK3β)—a key player dysregulated in AD [98]—leading to dramatic increases in APP and p-tau (reviewed in [89]). This evidence concerns the gene GSK3B and Alzheimer disease.