“Reassessing the Inflammatory Hypothesis of Alzheimer’s Disease: A Cross-Replication Mendelian Randomization Analysis of Interleukin Pathways”

Neuroinflammation is increasingly recognized as a key contributor to the pathogenesis of Alzheimer’s disease (AD). Circulating cytokines, particularly interleukins (ILs), play critical roles in immune signaling pathways that regulate neuroinflammatory processes, amyloid plaque formation, and neuronal injury.Observational studies have reported associations between systemic inflammatory markers and AD risk or progression; however, these studies are limited by confounding and reverse causation.To explore the potential causal role of inflammatory pathways, this study aims to systematically evaluate the causal associations between genetically predicted circulating levels of multiple interleukins and the risk of Alzheimer’s disease using a Mendelian randomization (MR) approach.