mice, which normally die by 20 weeks, can rescue these animals and restore both normal CNS myelination and neurological phenotype, a capability that may provide a basis for their use in therapeutic remyelination across a broad range of demyelinating disorders (Wang et al., 2013; Windrem et al., 2008). In particular, one may readily envisage that efforts now underway using tissue-derived cells to treat myelin disorders as varied as Pelizaeus-Merzbacher disease in children (Gupta et al., 2012), and chronic progressive multiple sclerosis in adults, may soon be supplanted by hESC and hiPSC-derived glial progenitor cells. Beyond that, a broad set of both pediatric and adult white matter disorders, ranging from the leukodystrophies and autoimmune demyelination to vascular and age-related white matter loss, may be promising targets for glial progenitor cell-based remyelination, as might iatrogenic causes of demyelination such as radiation therapy (Fox et al., 2014; Piao et al., 2015).
