In AD, microglia cluster around beta-amyloid plaques highlighting their inability to clear beta-amyloid (Hickman et al., 2008; Liu et al., 2010). Microglia are also implicated in the neuroinflammatory component of AD etiology, including cytokine/chemokine secretion, which exacerbate disease pathology (Guillot-Sestier and Town, 2013). Furthermore, microglia expressed AD GWAS genes like TREM2 and CD33 likely play a role in AD progression. Thus, there is a pressing need to further our understanding of human microglia and the influence of both pathology and disease-associated genes on microglial function. Addressing this critical need, we report the effective and robust generation of human iPSC microglial-like cells (iMGLs) that resemble fetal and adult microglia and demonstrate their utility in investigating neurological diseases like AD.
