Risk of Alzheimer’s Disease and Environmental Bisphenol A exposure

Abstract Environmental bisphenol A (BPA) exposure and bioaccumulation is higher than expected levels. In the long run, continuing BPA exposure impairs synaptic transmission and contributes to BPA-induced cognitive impairment, while increasing type-two diabetes risk via promoting pancreatic β-cell death. BPA-insulin-Alzheimer's disease (AD) axis represents a neuro-endocrine disorder and is termed as "Type 3 Diabetes". BPA elevates oxidative stress and amyloid beta accumulation in the AD brain, while increasing neuroinflammation and tau-phosphorylation. Neuronal viability is protected at high glucose concentration and insulin resistance conditions by N-methyl-D-aspartate (NMDA) receptor antagonists. Interestingly, despite its NMDA receptor suppressive effect, BPA contributes to neurotoxicity. Conversely, improvement of NMDA receptor functions shows protective effects against BPA-induced neurotoxicity. Thus, the mechanism of BPA neurotoxicity remains to be clarified.