Microglia activation and gliosis formerly were considered secondary to neurodegeneration in AD, however, recent genetic studies in late-onset AD implicate microglia- and astrocyte-related pathways in disease pathogenesis.[10, 48, 49] One focus of interest is TREM2, an innate immune receptor expressed on microglia and myeloid cells [50, 51]. This evidence concerns the gene TREM2 and Alzheimer disease.