Just as human glial chimeras may prove useful models by which to assess the role of glia in human cognitive processing, our ability to construct those mice with glia generated from human embryonic stem cells and induced pluripotential cells allows us to now establish human glial chimeras mice with glia derived from single patients (Figure 4), and from defined disease genotypes and phenotypes. That capability promises to significantly advance our understanding of the contributions of glia to the pathogenesis of a wide variety of neurological disorders, many of which have hitherto simply been assumed to be entirely neuronal in nature. For instance, the derivation of human GPCs from embryonic stem cells or induced pluripotential cells carrying the polyglutamine repeat expansion of Huntington disease (HD), and the establishment of human glial chimeras using those huntingtin mutant hGPCs, may permit us to define the specific contributions of glia to the neuropathology and clinical phenotype of HD. Similarly, our understanding and therapeutic modeling of disorders such as amyotrophic lateral sclerosis (ALS), already reported to derive in part from astrocytic pathology (Di Giorgio et
