Microglia genes are implicated in late onset AD, yet how they modify disease risk remains largely unknown. Thus, iMGLs were utilized to begin investigating how these genes might influence microglia function and AD risk. Hierarchical clustering using just these 25 AD-GWAS genes also demonstrates that iMGLs resemble microglia and not peripheral myeloid cells (Figure 4A). In their investigated basal state, iMGLs and microglia express many AD-GWAS-related genes including those without murine orthologs i.e. CD33, MS4A4A, CR1. Thus, iMGLs can be used to study how altered expression of these genes influence microglia phenotype in a way that cannot be recapitulated in transgenic mice. Therefore, iMGLs were used to investigate the influence of fAβ or BDTOs on AD-GWAS gene expression in microglia (Villegas-Llerena et al., 2015). Following fAβ exposure, iMGLs increased expression of 10 genes (Table S3) including ABCA7 (5.79 ± 0.44), CD33 (6.02 ± 0.41), TREM2 (4.86 ± 0.50, and APOE (2.52 ± 0.19), genes implicated in Aβ clearance/degradation. BDTOs increased expression of 4 genes including CD2AP (4.62 ± 0.45), previously implicated in tau-mediated toxicity (Shulman et al., 2014). In addition,
