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 of normal subjects, and transplanted these cells into immunodeficient neonatal mice to produce patient-specific human glial chimeric mice. The glial chimeric mice were then analyzed in regards to the effects of SCZ derivation on astrocytic and oligodendrocytic differentiation in vivo, as well as on behavioral phenotype, and the data thereby obtained correlated to disease-associated gene expression (Figure 1).
