Bisphenol A Treatment Impairs Synaptic Function in Human Cholinergic Neurons

Bisphenol A (BPA) is a synthetic compound widely used in the production of polycarbonate plastics and epoxy resins, commonly found in food and beverage packaging. Exposure to BPA can occur through several routes, although the primary source is dietary. Due to its ability to cross the placental and blood−brain barriers, the adverse effects of BPA can have implications across the entire human lifespan, from embryonic development to adulthood. While its harmful effect on brain development and function has been extensively documented in animal models, its impact on human mature neurons, particularly concerning synaptic activity, remains poorly understood. In this study, we investigated the effects of BPA on a human cholinergic neuron model. BPA exposure was found to reduce neuritic complexity and alter the expression of key synaptic proteins. These structural changes were accompanied by dysregulation of activity-regulated gene expression, indicating impaired synaptic function. Our findings suggest that even a short-term exposure to BPA can disrupt synaptic integrity, with potential consequences for normal brain functions.