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le ra w linating disease of the CNS that is distinguished by recur- of purified OPCs in a relatively short time is highly desir-the most recently published protocols (Wang et al., 2013; Stacpoole et al., 2013). Furthermore, O4+ OPCs wereYamada et al., 2014). iPSC-derived oligodendrocyte pro- We aimed to develop an efficient differentiation protocol es of oligo-nate and rescue a hypomyelinated mouse model, raising the possibility of future clinical trials (Wang et al., 2013). dendrocyte specification as it occurs in the spinal cord. In this process, PAX6+ neural stem cells give rise to OLIG2+genitor cells (OPCs) were shown to successfully remyeli- that recapitulates the critical developmental stagtargeting the immune system are highly effective at reducing or even stopping the intermittent episodes of inflammation, but they do not influence the course of pro-gressive MS. Therapeutic options for PPMS patients are limited to symptomatic treatments and the long-term prognosis is generally poor (Rice et al., 2013). Clearly, the unsolved challenge in the MS field is to develop neuropro-tective and remyelinating strategies for the treatment of progressive MS patients (Hauser et al., 2013). The genera-tion of patient-specific cells from induced pluripotent stem cells (iPSCs) or somatic cell nuclear transfer has recently emerged as a promising strategy for the develop-ment of autologous cell therapies (Goldman et al., 2012; able to differentiate into MBP+ mature oligodendrocytes in vitro and to myelinate axons in vivo when injected into immunocompromised shiverer (shi/shi) mice. No abnormal growths were observed. Our results provide a proof of concept that transplantation of iPSC-derived, pa-tient-specific cells for remyelination is technically feasible