This lapse has in large part been due to the lack of animal models of human glial pathophysiology: mouse brains have mouse glia. We therefore asked whether this limitation might be addressed using a novel model of human glial chimeric mice (Goldman et al., 2015; Han et al., 2013; Windrem et al., 2008) paired with the development of protocols for generating bipotential astrocyte-oligodendrocyte glial progenitor cells (GPCs) from patient-specific human induced pluripotent stem cells (hiPSCs) (Wang et al., 2013). In these human glial chimeric mouse brains, the majority of resident glia are replaced by human glia and their progenitors (Windrem et al., 2014), allowing human glial physiology, gene expression, and effects on neurophysiological function to be assessed in vivo, in live adult mice (Han et al., 2013). In this study, we used this glial chimeric model to assess the contribution of human glia to schizophrenic disease phenotype. To this end, we prepared hGPCs from iPSCs derived from fibroblasts taken from either juvenile-onset schizophrenic (SCZ) patients or their normal controls, assessed the differential gene expression of SCZ hGPCs relative to those
