(Figure 4), and rescuing at least a fraction of neonatally-engrafted shiverer mice from otherwise certain death (Wang et al. 2013). Yet while these hGPC differentiation protocols were developed so as to scale up production of hGPCs to clinically-useful levels, the ramifications of this capability on our understanding of the role of glia in brain function may prove profound. In particular, our ability to generate glia from human embryonic stem cells and induced pluripotential cells allows us to establish human glial chimeras using glia produced from individual patients, on a disease-specific basis, and to use those chimeric mice to assess the specific pathology of the disease-derived glia, as well as their broader contributions to disease pathogenesis. By way of early example, Fossatti and colleagues produced hGPCs from iPSCs derived from patients with primary progressive multiple sclerosis (PPMS), prepared and separated the oligodendrocyte-restricted daughter cells from these cultures, and then transplanted the immature oligodendroglia into shiverer mice, in which the cells differentiated as myelinogenic cells that ensheathed resident axons (Douvaras et al. 2014; Fossati and Douvaras 2014). While the analysis was too early to identify any stigmata of PPMS, the authors were able to report success in the establishment of mice chimerized
