their ability to produce mature neural phenotypes have been largely discredited. As such, the use of MSCs would seem logically limited to short-term immune modulation in settings for which pharmacological immune suppression has been found ineffective or otherwise ill-advised, such as SCI and stroke (DePaul et al., 2015; Liu et al., 2014). That, as well as the unclear mechanisms by which MSCs exert their immunosuppressive actions and the variability of those effects as a function of disease environment and duration, all serve to limit the utility of MSCs as clinical therapeutics. Whereas they may well prove beneficial in accelerating recovery from acute conditions exacerbated by central inflammation, such as stroke and relapsing multiple sclerosis - in each of which they are already under clinical assessment (Cohen, 2013; Hess et al., 2014; Rosado-de-Castro et al., 2013; Vu et al., 2014) – their efficacy in preserving threatened neurons and glia after acute injury, or improving the ultimate extent of functional recovery, remains unproven. In that regard, the more recent use of MSCs and related umbilical cord stem cells in largely non-inflammatory and structural conditions such as cerebral palsy (Englander et al., 2015), and in the genetic non-metabolic disorders of myelin such as
