STAT3 and Alzheimer disease: Furthermore, correlation analyses were conducted to elucidate potential interactions between three key hub genes showing prominent differential expression and these dysregulated pathways, with detailed associations depicted in Figure 9B. This comprehensive approach identified critical pathway alterations involving cytokine signaling (IL6-JAK-STAT3, TNFA-NFκB), redox homeostasis (Reactive Oxygen Species), and oncogenic regulation (MYC Targets V1/V2, PI3K-AKT-mTOR), collectively suggesting multifaceted pathophysiological disruptions in AD progression.