However, AD risk variants of TREM2 (e.g., TREM2 R47H, homozygous mutations or deletions, and heterozygous expression of TREM2 variants) impair the proper function of microglia in terms of phagocytosis, inflammatory response, energy metabolism, plaque compaction and activation, affecting disease progression (Ulland et al., 2017; Yin et al., 2017; Zhong et al., 2017). This evidence concerns the gene TREM2 and Alzheimer disease.