In summary, we have evidenced a continuous increased production of inflammatory mediators IL‐1β, p40, iNOS, and chemokines in AD models (Fig. 6), but no anti‐inflammatory cytokines such as IL‐4 and IL‐10, indicating that microglia/MDM do not shift toward an alternative anti‐inflammatory phenotype during the pathology. This evidence concerns the gene IL1B and Alzheimer disease.