Abstract: Bisphenol A (BPA), a widespread environmental endocrine disruptor, has been implicated in neurodevelopmental disorders, including Attention-Deficit/Hyperactivity Disorder (ADHD), through interfering with the human nervous system. However, the neurotoxic effects of BPA-induced ADHD and the underling mechanisms remain to be fully elucidated. This study employs network toxicology and molecular docking approaches to uncover the potential toxicological targets and molecular mechanisms of BPA-induced ADHD. First, potential toxicological targets of BPA were predicted using ChEMBL, STITCH, and Swiss Target Prediction platforms, while ADHD-related targets were compiled from the OMIM and GeneCards databases. Common potential targets were identified via Venn analysis. Subsequently, protein-protein interaction (PPI) networks were constructed using STRING and visualized in Cytoscape to identify core targets. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were performed using DAVID. Finally, molecular docking via the CB-Dock2 platform was employed to evaluate the binding interactions between BPA and the identified core targets. The results are summarized as follows: (1) A total of 408 BPA-related toxicological targets and 5134 ADHD-associated targets were identified, and 236 potential targets linked to both BPA exposure and ADHD were confirmed. (2) Thirty-nine core targets were identified via PPI network analysis, among which the top five key core targets are AKT1, HSP90AA1, HSP90AB1, ESR1 and MAPK3. (3) GO and KEGG analyses revealed significant enrichment in biological processes and signal pathways, including neuroactive ligand-receptor interaction, endocrine resistance, PI3K/Akt signaling pathway, MAPK signaling pathway, and FoxO signaling pathway. (4) Molecular docking confirmed strong binding affinities between BPA and five key core targets. This study reveals that BPA exposure may represent a critical environmental risk factor for ADHD and uncovers potential molecular mechanism through network toxicology and molecular docking. These findings provide a mechanistic framework for BPA neurotoxicity and may inform the development of targeted interventions for ADHD prevention.