the host glial network they are intended to replace. In particular, the extent to which the development of astroglial morphological and functional phenotype in the adult brain is cell-autonomous or context-dependent remains unclear. Nonetheless, in all of the disorders noted, we can reasonably expect that allografted human glial progenitors may prove effective at widespread remyelination and concurrent metabolic correction, the latter having already been established by Snyder and colleagues in mouse models using allografted neural stem cells (Lacorazza et al., 1996; Lee et al., 2007; Snyder et al., 1995). Combined with gene editing technologies to correct underlying mutations (Li et al., 2014), one might then anticipate the use of gene-edited human iPSCs and their derived glial progenitor cells in autologous therapy of affected children, across a broad range of pediatric leukodystrophies.
