Azadirachta indica (A. indica) has shown potential in treating Alzheimer's disease (AD) due to its bioactive compounds. However, the precise molecular mechanisms underlying their therapeutic effects remain insufficiently understood. Therefore, this study aims to elucidate the mechanisms of action of A. indica in the treatment of AD through an integrated approach involving network pharmacology and molecular docking analyses. Bioactive compounds of A. indica were obtained from IMPATT and PubChem, and potential targets were identified using SwissTargetPrediction. AD-related targets were retrieved from GeneCards, CTD and DisGeNET databases. Protein–protein interaction (PPI) networks were constructed using STRING and visualized in Cytoscape to identify hub genes via the CytoHubba plugin. Common targets were analyzed through Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment using DAVID. Finally, molecular docking was performed to assess binding interactions between active compounds and target proteins. Our analysis identified 3 active compounds (Nimbolide, Meliantriol, and Vilasinin), 36 therapeutic targets, and 11 hub genes, with 5 key hub genes including APP, EGFR, mTOR, PPARG, and GSK3B, were associated with the PI3K-Akt, ErbB, Neurotrophin, and HIF-1 signaling pathways, and were involved in functions including protein binding, ATP binding, and kinase activity of AD. molecular docking revealed that 3 compounds exhibited favorable binding affinities with the top 5 hub genes. The study revealed that the A. indica-mediated treatment of AD is a multifaceted process involving multiple bioactive compounds, molecular targets, and signaling pathways. These findings provide valuable insights into the potential molecular mechanisms through which A. indica exert their therapeutic effects on AD.