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Multiple sclerosis is thought to be partly an autoimmune and partly a neurodegenerative condition. For some reason, the body's immune system starts to mistakenly attack cells within the central nervous system. Initially the body can repair the damage to some extent, but with time nerve cells may begin to die.


Myelin is a fatty protein that forms a sheath around the axon of a nerve cell, the long thin part of the cell that transmits electrical messages. Myelin acts as insulation and helps maintain the speed of transmission of messages. In the central nervous system, myelin is produced by cells called oligodendrocytes. Part of the attack by the immune system in MS is directed at myelin.


The process of damaging or stripping away myelin from an axon is called demyelination. Messages that pass along a demyelinated nerve become delayed or blocked. As the central nervous system controls processes throughout the body, a wide range of symptoms can occur, depending on where the nerve damage has happened. For example, damage to areas in the spinal cord can lead to problems with mobility or weakness.


Once the inflammation caused by the immune attack is over, it is possible for the body to replace damaged myelin, a process known as remyelination. Whether this happens or not depends on whether there is damage to the surrounding oligodendrocytes, the supporting cells that produce myelin and which are also attacked by this process. Although the new myelin can work effectively, it tends to be thinner than unaffected myelin and so messages through the affected nerves may not be as fast as before the attack.

Remyelination tends to occur in the earlier stages of MS but, with repeated attacks, oligodendrocytes are damaged and destroyed and myelin is not as easily replaced. If an axon is left without the protection of myelin it will be more vulnerable to damage and may die.

diagram of damage to a nerve cell


The central nervous system is able to overcome small areas of axon loss by finding ways to reroute messages around an area of damage using undamaged nerve cells. This ability to adapt to avoid areas of damage is called plasticity. Messages may take longer to get through but symptoms will improve to some extent.

Should the area of damage become too large, this rerouting process is no longer able to compensate and messages to or from that part of the central nervous system are permanently blocked, resulting in symptoms that do not improve.


Scar tissue may develop on the damaged nerve. The forming of scar tissue over areas of damaged myelin is what forms the lesions or scarring ('sclerosis') that show up as white regions on MRI scans.

Neuroprotection and myelin repair

Neuroprotection is an area of research that aims to develop drugs that protect nerves from damage and so halt or slow down the progression of MS. If drugs could be developed that promote myelin repair, then damage could be reversed and function improved.


  • Compston A, et al. McAlpine's multiple sclerosis. 4th ed. London: Churchill Livingstone;2006.

Last updated: 21 September 2015
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