o l

ls p e e g sp by relevant and unequivocal animal stud-ies. One adverse clinical advent could and colonize the brain during early devel-opment (Kessaris et al., 2006). This cell opmental cues that regulate oligodendro-cyte production and myelination. Mostsubstantially delay further development of this promising therapeutic approach for treating human diseases of myelin. In this issue, Dr. Stephen Goldman’s laboratory provides a compelling ‘‘proof-of-principal’ ’ animal study that addresses several critical issues facing the develop-ment of future clinical trials in humans (Windrem et al., 2008). In this study, hu-man oligodendrocyte progenitor cells (OPCs) were transplanted into the CNS of newborn ‘‘shiverer’ ’ mice that lack my-elin basic protein (MBP), a major protein constituent of CNS myelin. Due to the type is the only known source of oligoden-drocytes and represents a significant glial cell population in the adult brain. Windrem and colleagues isolated oligodendrocyte progenitors from human fetal brain by panning with A2B5 antibodies. Similar selection techniques have been used to obtain this population for decades, and much is known about their behavior in vivo, in vitro, and after transplantation into animal models of myelin disease (for review, see Baron-Van Evercooren and Blakemore, 2004). Several methodological differences importantly, the donor oligodendrocytes can successfully compete with the defec-tive host oligodendrocytes. Since most human myelination occurs postnatally, the microenvironment of the neonatal brain is not significantly altered by dys-myelination. This is relevant to the design of human studies, because chronic dys-myelination can cause astrocytic scars that may inhibit OPC migration and oligo-dendrocyte differentiation. In addition, chronically dysmyelinated axons can be-come dystrophic and degenerate. The neonatal brain, therefore, appears to beRescue of Conge