Figure 8
Hypothetical model of BPA-induced Alzheimer’s disease-like neurotoxicology. BPA disturbs the insulin signaling pathways by decreasing IR tyrosine phosphorylation and increasing IRS1 serine phosphorylation, which leads to reduced AKT phosphorylation. The inactivation of AKT subsequently results in the overactivation of GSK3α and GSK3β, two critical enzymes responsible for APP and p-tau formation. APP is subsequently hydrolyzed by BACE-1, which facilitates Aβ1–42 generation, and the increased Aβ1–42 expression and enhancement of p-tau result in an AD-like disease.
