<p>Alzheimer’s Disease (AD) is a multifactorial neurodegenerative disorder marked by persistent neuroinflammation and dysregulated signalling pathways. This study investigates AD-associated molecular pathways using bioinformatics analysis and explores the potential role of vincamine in multi-target therapy in AD. Microarray gene expression data from the GSE44770 dataset were analysed using GEO2R to identify differentially expressed genes (DEGs) between AD and control samples. Visualisation was performed using a volcano plot, Uniform manifold approximation and projection, and boxplot analyses. A protein-protein interaction network was constructed, and key hub genes were identified using CytoHubba based on degree, betweenness, and Maximal clique centrality. The transcription factor-target gene and miRNA-target gene regulatory network was constructed to explore upstream transcriptional and post-transcriptional regulation. Network pharmacology analysis was performed further to evaluate the therapeutic potential of vincamine with identified hub genes and associated signalling pathways of AD. A distinct transcriptomic difference was observed between the AD and control samples. Hub gene analysis consistently identified IL-6, TNF, IL-1β, and AKT1 as associated with inflammatory and signalling pathways. Transcription network analysis revealed STAT3 as an upstream regulator of major inflammatory mediators, and miRNA regulatory analysis identified hsa-miR-155-5p and hsa-miR-199a-3p as highly connected miRNAs, with coordinated regulators of STAT3 and AKT1. Network pharmacology analysis suggested that vincamine may interact with multiple hub genes and signalling pathways involved in neuroinflammatory, apoptotic, and survival-related mechanisms in AD. Bioinformatics and network pharmacology analysis identify STAT3, IL-6, and AKT1 as important inflammatory mediators and highlight vincamine as a potential multi-target therapeutic candidate for AD.</p>