Remyelination

Remyelination is the process of propagating oligodendrocyte precursor cells to form oligodendrocytes to create new myelin sheaths on demyelinated axons in the CNS. This is a process naturally regulated in the body and tends to be very efficient in a healthy CNS. The process creates a thinner myelin sheath than normal, but it helps to protect the axon from further damage, from overall degeneration, and proves to increase conductance once again. Demyelinating diseases, such as Multiple Sclerosis, have been of utmost interest within the last couple of decades. Recent research is uncovering some of the many unknown pathways involved with remyelination in hopes of battling demyelinating diseases like MS which can ultimately cripple a person. While no treatment exists yet in preventing remyelination failure in the chronic stages of these diseases, future research may yet prove to unlock key pathways that can be targeted.

Remyelination is activated and regulated by a variety of factors surrounding lesion sites that control the migration and differentiation of Oligodendrocyte Precursor Cells. Remyelination looks different from developmental myelination in the structure of the myelin formed. Reasons for this are unclear, but proper function of the axon is restored regardless. Perhaps of most interest are the inhibition and promotion factors of this physiological process. One way this process can be traced is by following different protein activation sequences which have shown just how quickly remyelination begins after injury (within a few of days).

The most notable evidence that remyelination has taken place on an axon is its thin myelin sheath created by an oligodendrocyte, though the reason why the new myelin sheath is thinner remains unclear. This can be quantified in the g-ratio, the ratio between the diameter of the axon itself to the outer diameter of the myelinated fiber. So then, this value will always be less than 1, but remyelinated axons tend to have values closer to 1 (indicating a thinner myelin sheath) than those myelinated naturally. The g-ratio differences are less apparent on smaller axons.

The thinner myelin not only restores protection of the axon from degradation, but also restores a faster conduction velocity. The conduction velocity, however, is not as strong as naturally myelinated axons and the Nodes of Ranvier are inclined to be wider which results in less coverage in the axon by myelin than what is natural.

...
Wikipedia