Since glial progenitor cells give rise to astrocytes as well as oligodendrocytes, and are highly migratory – they typically distribute throughout the neuraxis after perinatal graft, and can do so well into adulthood – these cells may also be of great utility in rectifying the dysmyelination-associated enzymatic deficiencies of the pediatric lysosomal storage disorders, such as Krabbe disease, metachromatic leukodystrophy Tay-Sachs disease, and the mucopolysaccharidoses, among others, as well as the astrocytic pathology of vanishing white matter disease (Goldman, 2011). To be sure, substantial heterogeneity in both astroglial ontogeny and phenotype has been noted (Bayraktar et al., 2015; Chaboub and Deneen, 2012; Schitine et al., 2015; Zhang and Barres, 2010), most especially so in the adult human forebrain (Oberheim et al., 2006; Oberheim et al., 2009), and it remains unclear how precisely engrafted glial progenitors can recapitulate the pleomorphism of 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,
