Although animal models report seemingly conflicting effects of eliminating or overexpressing Trem2 [113,114], and the relative contribution of peripheral and CNS-resident cells is yet to be investigated, most studies agree that the receptor (and by extension, myeloid cells) plays an important role in the response to deposition of Aβ in AD, likely though effects on cell surface transport and phagocytosis [115,116]. This evidence concerns the gene TREM2 and Alzheimer disease.