pose a useful, and potentially intriguing, model for assessing the specific contributions of human astroglia to schizophrenic behavioral and cognitive pathology. In broader terms, such disease-specific iPSC-derived human glial chimeras may permit us to better define the role of glial dysfunction in a broad swath of neurodegenerative and neuropsychiatric disorders, in which the relative contributions of glial pathology remain unclear, and for which the corrective targeting of glial dysfunction may prove a highly promising therapeutic opportunity.
