It is already known that a soluble form of TREM2 (sTREM2) derived from proteolytic cleavage of the cell surface receptor is increased in the preclinical stages of AD, positively correlates with the amounts of total and phosphorylated tau in the cerebrospinal fluid, promotes microglial survival in a PI3K/Akt-dependent manner, and stimulates the production of inflammatory cytokines depending on NF-κB. This evidence concerns the gene TREM2 and Alzheimer disease.