Previous studies in our laboratory, examining the role of brain inflammation in AD pathology, revealed that chronic, low level expression of IL-1β in the brain of GFAP-IL1βXAT; APP/PS1 compound transgenic mice resulted in amelioration of AD pathology via removal of Aβ plaques following the recruitment of peripheral immune cells in the brain [19,39]. This evidence concerns the gene IL1B and Alzheimer disease.