The cells responsible for building and maintaining the myelin sheath, the protective coating the surrounds the neurons, are being studied by researchers looking for possible treatments for multiple sclerosis. In multiple sclerosis, this myelin sheath is diminished, destroyed by the body's immune system. The lack of this protective coating hampers communication between the brain and the body; moreover, without the protection that myelin provides, the nerves themselves are likely to be damaged over time, often irreversibly.
Multiple sclerosis is an autoimmune disease, in which the immune system attacks the body's own tissue as though it were an infection. As with most autoimmune diseases, there's a strong genetic component, but the disease itself is generally triggered by certain life experiences—in the case of multiple sclerosis, that means certain infectious diseases, such as Epstein-Barr.
The treatment typically involves using corticosteroids to help with the inflammation and any of several types of drugs, such as beta interferons, to refuse the frequency and severity of attacks and to try to slow the progression of the condition. Muscle relaxants and other medications are administered during attacks to alleviate the symptoms. However, there is no cure for the condition; patients must rely on getting exercise, staying well-rested, keeping cool, avoiding stress, and eating a healthy diet to keep attacks at bay.
Researchers, however, are embarking on studies that may lead to more effective and longer-term treatments. They're looking at oligodendrocytes, the cells responsible for producing myelin in the first place. In the lab animals being studies, these cells only produce myelin for about five hours. If human oligodendrocytes have a similar time limit, it's possible that attempts to overcome it—either by reactivating the cells or by creating new ones may help directly restore the myelin sheath. This would be a reversal of the disease process itself, treating the condition directly rather than attacking its effects.