human GPCs and their derived astrocytes. That said, our observations of significant defects in SCZ glial maturation shared by hGPCs derived from multiple independent patients, associated in each with hypomyelination and disrupted astrocytic differentiation, as well as with abnormal behavioral phenotypes in the resultant SCZ GPC chimeras, together suggest a strong causal contribution of glial pathology to schizophrenia. In addition, these data highlight the potential of disease-specific humanized chimeras in defining the respective contributions of glial and neuronal dysfunction in the genesis and course of neurological disease.
