Paradoxical associations (e.g., eotaxin-2, IL-2R with better memory) and APOE ε4-linked immune differences indicated context-dependent roles.<h4>Discussion</h4>This exploratory study reveals biologically plausible, inflammatory heterogeneity in AD and highlights plasma cytokine profiles as candidate biomarkers and therapeutic targets, warranting investigation. This evidence concerns the gene CCL24 and Alzheimer disease.