• • Identified six key toxic proteins (TP53, HSP90AA1, HSP90AB1, INS, BCL2, AKT1) common to BPA-induced AD, PD, and HD; BCL2 is the most central hub, indicating a convergent apoptotic mechanism across diseases.
• • BPA exposure induces oxidative stress and cell cycle arrest in SVGP12 astrocytes, leading to mitochondrial apoptosis via inhibition of INS-AKT1-BCL2 and activation of TP53-HSP90 pathways, disrupting neural homeostasis.
• • The study integrates network toxicology, molecular docking, and molecular dynamics simulations, providing a multi-scale approach to predict and validate BPA neurotoxicity, surpassing traditional single-target analyses.
• • The findings establish a mechanistic link between BPA and three major neurodegenerative diseases, offering a unified target set for therapeutic intervention and risk assessment of BPA-related neurotoxicity.