The limited repair capacity of the adult human brain further compounds this complexity. Despite the persistence of somatic neural stem cells and neuronal progenitor cells in the adult human brain (Arsenijevic et al., 2001; Eriksson et al., 1998; Ernst et al., 2014; Kirschenbaum et al., 1994; Pincus et al., 1998; Roy et al., 2000; Sanai et al., 2004), little evidence exists as to the contribution of these cells to structural repair in adult humans. In the early days of stem cell biology, reports appeared of context-dependent differentiation of transplanted pluripotent stem cells (PSC) or neural stem cells (NSCs) into phenotypes of interest or need (Liu et al., 2000), but realization soon grew that such demand-based differentiation was limited in scope. Rather, it became evident that for disorders of specific neuronal and glial phenotypes, that the deficient cell types or their immediate progenitors would need to be introduced to achieve structurally-accurate repair. In particular, it became clear that repair of the injured or diseased brain required the upfront determination of which cellular phenotypes, at which stages of their development, were most
