Class 3 semaphorins influence oligodendrocyte precursor recruitment and remyelination in adult central nervous system.

Oligodendrocyte precursor cells, which persist in the adult central nervous system, are the main source of central nervous system remyelinating cells. In multiple sclerosis, some demyelinated plaques exhibit an oligodendroglial depopulation, raising the hypothesis of impaired oligodendrocyte precursor cell recruitment. Developmental studies identified semaphorins 3A and 3F as repulsive and attractive guidance cues for oligodendrocyte precursor cells, respectively.

Axon-oligodendrocyte interactions during developmental myelination, demyelination and repair.

In multiple sclerosis, CNS demyelination is often followed by spontaneous repair, mostly achieved by adult oligodendrocyte precursor cells. Extent of this myelin repair differs, ranging from very low, limited to the plaque border, to extensive, with remyelination throughout the 'shadow plaques.' In addition to restoring neuronal connectivity, new myelin is neuroprotective.

Remyelination in multiple sclerosis.

Remyelination in multiple sclerosis is in most cases insufficient, leading to irreversible disability. Different and nonexclusive factors account for this repair deficit. Local inhibitors of the differentiation of oligodendrocyte progenitor cells (OPCs) might play a role, as well as axonal factors impairing the wrapping process.

Semaphorin 3A and 3F: key players in myelin repair in multiple sclerosis?

The presence of demyelinated plaques in the central nervous system is the hallmark of multiple sclerosis (MS). Some plaques remyelinate but others do not, leaving permanent damage. The reasons for this failure of repair are many, but one possible reason is the lack of migration of oligodendrocyte precursor cells to the lesion.

Astrocytes--friends or foes in multiple sclerosis?

In multiple sclerosis (MS), the presence of demyelinating plaques has concentrated researchers' minds on the role of the oligodendrocyte in its pathophysiology. Recently, with the rediscovery of early and widespread loss of axons in the disease, new emphasis has been put on the role of axons and axon-oligodendrocyte interactions in MS. Despite the fact that, in 1904, Müller claimed that MS was a disease of astrocytes, more recently, astrocytes have taken a back seat, except as the cells that form the final glial scar after all hope of demyelination is over.