In patients with Multiple Sclerosis, spontaneous repair mechanisms can be observe, allowing the synthesis of a new functional myelin sheath. Unfortunately, these regeneration processes are insufficient to allow functional recovery. In this context it is important to better understand these mechanisms and to identify strategies to promote them. Pascale Durbec’ team showed, in an experimental model of demyelination in mice, that neuroblasts from adult brain stem cells can participate in this repair. The team’s shows that forced expression of two transcription factors, Olig2 and Sox10, is sufficient to induce reprogramming of neuroblasts into oligodendrocytes and promote the repair process in animals.  These studies are a first step towards the development of therapies for patients with multiple sclerosis.

A) In the adult rodent brain, neural stem cells in the sub-ventricular zone (SVZ) generate neuroblast cells (Nbs) that migrate through the rostral migration stream (RMS) to the olfactory bulb (OB) where they differentiate into neurons. B) After lesion, some rare Nbs (in red) can spontaneously trans-differentiate into oligodendrocyte progenitor cells. C) The ectopic expression of Olig2 and Sox10 increases the number of cells that change their fate and differentiate into myelinating oligodendrocytes (green). Thus this strategy promotes the repair process in the demyelinated corpus callosum.

A) In the adult rodent brain, neural stem cells in the sub-ventricular zone (SVZ) generate neuroblast cells (Nbs) that migrate through the rostral migration stream (RMS) to the olfactory bulb (OB) where they differentiate into neurons. B) After lesion, some rare Nbs (in red) can spontaneously trans-differentiate into oligodendrocyte progenitor cells. C) The ectopic expression of Olig2 and Sox10 increases the number of cells that change their fate and differentiate into myelinating oligodendrocytes (green). Thus this strategy promotes the repair process in the demyelinated corpus callosum.

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