As AD progresses, microglia appear to become progressively dysfunctional; TREM2 becomes down-regulated and microglia lose their ability to clear Aβ42 peptides while producing and releasing neurotoxins, reactive oxygen species (ROS), and pro-inflammatory cytokines that further promote Aβ42 production and pathological aggregation (Schmid et al., 2002; Alexandrov et al., 2013; Boutajangout and Wisniewski, 2013; Hickman and El Khoury, 2013). This evidence concerns the gene TREM2 and Alzheimer disease.