MS Society supported study yields new information on "remyelination"

Background: Remyelination and MS

Multiple sclerosis symptoms are the result of damage to myelin, a substance which wraps around and protects the wire-like structures known as axons which are found in the brain, spinal cord and optic nerve. Myelin also serves as an insulator for axons, allowing them to send nerve impulses required by the body to see, walk, write, speak, and other basic functions. When myelin is damaged, the speed with which axons deliver nerve impulses is either slowed dramatically or lost completely.

During normal development, a group of cells called oligodendrocytes are responsible for producing myelin. Because of their critical role in myelin production, oligodendrocytes have been intensively investigated by researchers to see if they are able to reform damaged myelin after an immune attack in MS, through a process known as ‘remyelination’. Previous evidence has demonstrated that remyelination can and has occurred in the central nervous system of people with MS. Now they are trying to determine which cells are responsible for creating new myelin, and if the level of remyelination is sufficient to repair what has been lost in MS.

MS Society of Canada funded scientist and clinician Dr. Jack Antel has been leading a lab of MS researchers from McGill University who actively explore remyelination through a series of elaborate cell, animal and human experiments. Their latest research, published in the American Journal of Pathology, suggests that oligodendrocyte precursor cells (OPCs) - the younger version of oligodendrocytes - may actually be the source of new, healthy myelin in MS following immune-mediated damage.

Study Methods and Results:

Dr. Antel and colleagues conducted a series of laboratory experiments comparing the presence and remyelination capabilities of oligodendrocytes versus their younger counterparts, the OPCs. These experiments used tissue samples taken from people with MS as well as healthy volunteers.

Summary of results:

  1. When they compared tissue samples from people with MS versus samples from healthy volunteers, researchers noticed that OPCs took a harder hit than oligodendrocytes when under attack.
    • This was reflected by a greater reduction in numbers of OPCs versus oligodendrocytes and suggests that OPCs may be more vulnerable to the destructive activity of immune cells in MS
  2. OPCs were able to travel to sites of damage to begin repairing injured tissue
    • This further implies the role of OPCs in promoting remyelination in MS
  3. When oligodendrocytes were added to the MS cell cultures, the oligodendrocytes failed to produce myelin.
    • This suggests that oligodendrocytes are not the main source of repair
  4. When OPCs were removed from the MS cell cultures, remyelination failed to occur.
    • This suggests that OPCs are required for repair of MS lesions

Relevance:

This new data demonstrates that the younger oligodendrocytes - the oligodendrocyte precursor cells or OPCs - may be more important in tissue repair following an MS relapse. In fact, this MS Society funded study proposes that damage to or loss of OPCs greatly contributes to the limited remyelination observed in MS, which in turn may lead to progression of disease. If research confirms these findings, there is strong potential for the development of MS therapies to stimulate activity or promote survival of OPCs with the goal of boosting their capacity for remyelination.

Source:
Cui Q et al. Oligodendrocyte progenitor cell susceptibility to injury in multiple sclerosis. American Journal of Pathology 2013 7 June [Epub ahead of print]