Objective To investigate the potential association between diethyltoluamide and the risk of vascular dementia (VaD), and to predict its core targets and molecular mechanisms using network toxicology and molecular docking. Methods The toxicological characteristics and potential targets of diethyltoluamide were predicted using toxicological databases. VaD-related targets were retrieved from disease databases. The STRING database was used to construct a protein-protein interaction network to screen core genes. Pathway enrichment analyses were conducted on the intersecting genes. Finally, the key protein was selected and its binding affinity with diethyltoluamide was verified through molecular docking technology. Results Network toxicology analysis identified 71 common targets of diethyltoluamide and VaD. Core targets included TNF, TP53, ACTB, HSP90AA1, and KRAS. These targets were enriched in cellular response to oxidative stress, inflammatory response, and apoptotic signaling pathway, as well as key signaling pathways including PI3K-Akt, mitogen-activated protein kinase. Molecular docking confirmed that diethyltoluamide exhibited strong binding affinity with these core targets. Conclusions Diethyltoluamide may participate in the pathological process of VaD by directly acting on multiple core targets such as TNF, TP53, and KRAS, thereby interfering with various pathways including neuroinflammation, oxidative stress, and cerebrovascular regulation.