The discovery of increased Alzheimer’s disease (AD) risk in carriers of rare Triggering Receptor Expressed on Myeloid Cells-2 (TREM2) mutations from genome-wide association studies [24, 31] jump-started the interest in characterizing the potential roles of TREM2 protein, and more generally innate immune function, in the progression of the disease. Here, TREM2 is linked to early-onset autosomal dominant Alzheimer disease.