This study employed an integrated network toxicology and molecular docking approach to explore the molecular mechanisms by which the herbicide 2,4-Dichlorophenoxyacetic acid (2,4-D) may contribute to neurodegenerative diseases (NDDs). We identified 89 common targets through the intersection of potential 2,4-D-related targets and NDD-associated genes. Among these, 12 core targets—including NFKB1, PPARG, SERPINE1, NOS3, and NFE2L2—were highlighted via protein–protein interaction network analysis. Functional enrichment revealed that these targets are involved in key pathways such as inflammatory response, oxidative stress, metabolic dysregulation, and synaptic dysfunction. Molecular docking further confirmed strong binding affinities between 2,4-D and all core targets (binding energy ≤ −5.1 kcal·mol⁻¹). These findings systematically reveal, for the first time, a multi-target and multi-pathway mechanism through which 2,4-D may induce neuronal injury, providing a theoretical basis for assessing environmental risk in neurodegeneration.