The discovery of inflammatory biomarkers, interleukin- (IL-) 1β [4, 5], and AD risk genes associated with innate immune function, apolipoprotein E (APOE) and triggering receptor expressed on myeloid cells 2 (TREM2), in AD patients suggests that neuroinflammation is essential in pathogenesis [2, 6]. This evidence concerns the gene TREM2 and Alzheimer disease.