Despite the intrinsic phenotypic heterogeneity of microglia, DAMs are functionally and pathologically distinct from their neurotypical counterparts: they express significantly lower levels of genes related to microglial homeostasis (including a host of purinergic receptors) and express far greater levels of genes associated with AD risk, including Apolipoprotein E (APOE), Lipoprotein lipase (LPL), and Triggering Receptor on Myeloid Cells 2 (TREM2) (Keren-Shaul et al., 2017; Ofengeim et al., 2017). This evidence concerns the gene APOE and Alzheimer disease.