Abstract
Myelin sheaths, by supporting axonal integrity and allowing rapid saltatory impulse conduction, are of fundamental importance for neuronal function. In response to demyelinating injuries in the central nervous system (CNS), oligodendrocyte progenitor cells (OPCs) migrate to the lesion area, proliferate and differentiate into new oligodendrocytes that make new myelin sheaths. This process is termed remyelination. Under specific conditions, demyelinated axons in the CNS can also be remyelinated by Schwann cells (SCs), the myelinating cell of the peripheral nervous system. OPCs can be a major source of these CNS-resident SCs—a surprising finding given the distinct embryonic origins, and physiological compartmentalization of the peripheral and central nervous system. Although the mechanisms and cues governing OPC-to-SC differentiation remain largely undiscovered, it might nevertheless be an attractive target for promoting endogenous remyelination. This article will (i) review current knowledge on the origins of SCs in the CNS, with a particular focus on OPC to SC differentiation, (ii) discuss the necessary criteria for SC myelination in the CNS and (iii) highlight the potential of using SCs for myelin regeneration in the CNS.
Highlights
Demyelinating diseases comprise a diverse spectrum of disorders including the autoimmune disease multiple sclerosis (MS) in the central nervous system (CNS), Guillain Barre syndrome in the peripheral nervous system (PNS), and genetic disorders such as leukodystrophies (CNS) and Charcot–Marie–Tooth disease (PNS)
We focus on the intriguing observation that Schwann cells (SCs), the myelinating cells of the PNS, can be detected in the CNS of multiple sclerosis (MS) [4,6,7], neuromyelitis optica [8] and in spinal cord injury patients [9,10,11]
We would expect that unopposed BMP and Wnt signalling will instruct oligodendrocyte progenitor cells (OPCs) to differentiate into SCs: unpublished work from our laboratory found no significant increase in SC-remyelinated axons following demyelination in Sostdc1 KO mice
Summary
Demyelinating diseases comprise a diverse spectrum of disorders including the autoimmune disease multiple sclerosis (MS) in the central nervous system (CNS), Guillain Barre syndrome in the peripheral nervous system (PNS), and genetic disorders such as leukodystrophies (CNS) and Charcot–Marie–Tooth disease (PNS). Direct damage to the myelin sheath or to the myelinating cells, oligodendrocytes in the CNS and Schwann cells (SCs) in the PNS, can arise in consequence to genetic mutations, trauma, metabolic deficiencies or exposure to inflammation or toxins [1]. In both the CNS and PNS, the loss of myelin sheaths from otherwise intact axons, termed demyelination, is followed by a spontaneous, regenerative response, called remyelination. While the need for remyelination therapies remains unmet, developing methods to harness the remarkable regenerative potential of myelinating glia represents an exciting avenue of research
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