Missense mutations of triggering receptor expressed on myeloid cells 2 (TREM2) are associated with an enhanced risk of developing dementia including late‐onset Alzheimer’s disease (LOAD).4, 5 In the CNS, TREM2 is exclusively expressed in microglia and numerous studies have linked the disease‐associated mutations to deficits in microglial function, including ligand binding/sensing, phagocytosis, and inflammatory responses.6, 7. This evidence concerns the gene TREM2 and early-onset autosomal dominant Alzheimer disease.