In that study, TREM2 overexpression reduced the accumulation of Aβ and the expression of BACE-1, Iba-1, GFAP, TNF-α, IL-6, and IL-1β in both the cortex and hippocampus in an APP/PS1 transgenic mouse model of AD and also led to the upregulation of M2 phenotype markers (Arg-1, IL-10, and Ym1) in both the cortex and hippocampus [114]. This evidence concerns the gene GFAP and Alzheimer disease.