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. This evidence concerns the gene TREM2 and Alzheimer disease.