Taking this approach further, we may anticipate the construction of human glial chimeras using hGPCs produced from iPSCs of patients with hereditary neuropsychiatric conditions, and the use of these mice to define and isolate the contribution of glia to these most enigmatic of brain disorders. Indeed, the phylogenetic appearance of one of the major neuropsychiatric disorders of humans, schizophrenia, seems roughly concurrent with the evolution of morphological complexity by human astroglia (Horrobin 1998; Oberheim et al. 2009) More broadly, this approach may be of particular value in assessing the role of glia in those neurological disorders that are fundamentally unique to humans, including not only schizophrenia, but also bipolar disease and autism spectrum disorders, whose phylogenetic appearances parallel that of human astrocytic evolution. By way of example, human glial chimeric mice established with hGPCs derived from schizophrenic patient-derived iPSCs may 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
