There was also an overall reduction in proinflammatory milieu in the hippocampus and cerebral cortex, which could be gleaned from reduced concentrations of NLRP3 inflammasome activation mediators (NF‐kB‐p65, NLRP3, ASC, and cleaved caspase‐1), end products (IL‐1β and IL‐18), and other proinflammatory cytokines such as TNFα, MIP1α, and IL‐6 in the hippocampus and cerebral cortex of the AD‐PLX group compared to the AD group. This evidence concerns the gene IL1B and Alzheimer disease.