of neuronal phenotypes lost, to recapitulate their specific patterns of connection to one another, and in the cortex, to reproduce the laminar organization and connectivity of the host brain. Similarly, the glial populations would need to be replaced, while the intricate relationship of parenchymal glia to neurons within their domains would need to be re-established, just as the neuronal axons would need to be remyelinated. The requirements for restoring tissue lost to stroke are thus so demanding that current strategies for cell replacement are simply insufficient. As more phenotypes can be independently generated an admixed before transplant, and as we gain more insight into the potential for self-organization among those phenotypes, we may hope for future advances in cell replacement for stroke. But for now and the decade to come, the likelihood of cell replacement evolving as a significant treatment modality for stroke and trauma would seem low. Perhaps in recognition of those difficulties, much work over the last decade has shifted to using neural and mesenchymal stem cells in stroke, not as agents for cell replacement, but rather as immunomodulators intended to suppress the post-ischemic inflammatory response (Aharonowiz et al., 2008; Kokaia et al., 2012). This is an approach
