Detection of molecular signatures and pathways shared by Alzheimer's disease and type 2 diabetes

Alzheimer's disease (AD) and type 2 diabetes (T2D) are common in the general elderly population, conferring heavy individual, social, and economic stresses on families and society. Accumulating evidence indicates T2D to be a risk factor for AD. However, the underlying mechanisms for this association are largely unknown. This study aimed to identify the shared molecular signatures between AD and T2D through integrated analysis of temporal cortex gene expression data. Gene Ontology (GO) and pathway enrichment analysis, protein over-representation analysis, protein-protein interaction, DEG-transcription factor interactions, DEG-microRNA interactions, protein-drug interactions, gene-disease association analysis, and protein subcellular localization analysis of the common DEGs were performed. We identified 16 common DEGs between the two datasets, which were mainly enriched in the biological processes of apoptosis, autophagy, inflammation, and hemostasis. We also identified five hub proteins encoded by the DEGs, five central regulatory transcription factors, and six microRNAs. Protein-drug interaction analysis showed C1QB to be associated with different drugs. Gene-disease association analysis revealed that hub genes, SFN and ITGB2, were actively engaged in other diseases. Collectively, these findings provide new insights into shared molecular mechanisms between AD and T2D and provide novel candidate targets for therapeutic intervention.