Essay on multiple sclerosis

Submitted By irishIJcastro
Words: 961
Pages: 4
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It is believed that MS is triggered in susceptible individuals via viral or bacterial infection that has an antigen, which mimics the MS "self antigen" on myelin. A macrophage then engulfs the pathogen. The "self-mimicking" antigen fragment derived from the pathogen is then displayed on the macrophage surface, along with a human lymphocyte antigen (HLA) molecule. If a circulating T cell recognizes the antigen-HLA complex, it will bind to it and undergo primary activation/ replication. The cloned T-cells travel around the body and attack any cells that bear the "self-mimicking" antigen. Activated T cells bind to the epithelial walls of the brain by releasing cytokines (mediator cells) such as interferon gamma and lymphotoxin. These regulate the production of complementary adhesion molecules to the cohesion molecules on the walls of the brain, causing T-cells to bind to them. Within the CNS, the cytokines released by the T-cells act on microglia, transforming them into antigen-presenting cells capable of displaying myelin fragments. These T-cells, activated to attack the myelin-mimicking antigen, bind to the myelin microglia and undergo secondary activation. After another round of proliferation, new T-cells bind to microglia and cause the release of more and more cytokines. At this time there is more and more binding of the T-lymphocytes occurring to microglia. This chaos of chemicals causes the inflammation of the blood-brain barrier, thinning it so that T-cells, B-cells and macrophages may enter. Macrophages complete the process by stripping the myelin sheath directly off the nerves. In turn, they release necrosis factor alpha, which is believed to damage oligodendracytes - the cells that produce myelin - making the damage irreparable. (2) The replication of T-cells, the secretion of more and more cytokines, and the eventual destruction caused by the macrophages is cyclic. The myelin can be come inflamed, swollen, or even detached from the nerve fibers. Eventually, it is destroyed and hardened patches of scar tissue form over the fibers (5).

The acceptance of the auto-immune theory has dominoed into the type of treatments available for MS. Because cytokines are the cause of much of the damage upon the glial cells during the immune attack, researchers have sought out ways to suppress the inflammatory response. One newly FDA approved drug therapy used to treat MS is thalidomide, which has anti-inflammatory and immunosuppressant effects making it ideal for these conditions (7). Marketed in the past as a mild sedative, it was pulled off the drugstore shelves when it was proven to cause dangerous birth defects in pregnant women (7). Another drug therapy utilized to treat MS is methprednisolone, a synthetic adrenal steroid hormone, which has powerful effects on suppressing inflammation. Shortening any flare-ups of MS, the drug does not permanently retard progression of the disorder (4). Newer drugs hold greater promise of beneficial effects. Many of them are beta-interferons, which reduce the frequency of flares by about 30% by reducing the number of cytokines in the brain (4). The three forms of treatment stated above seem to be the most recent and well-prescribed by physicians who treat victims of MS. Upon searching the Internet further, it was found that there were hardly any treatments for patients with MS that were not pharmacological. One homeopathic treatment of MS dealt with strengthening the blood-brain barrier (BBB), such that no immune cells could pass through. Not approved by the FDA, it was a suggestion found on a personal home page of a man concerned with treatments for MS. He believed that the increase of flavonoids in a person’s diet would strengthen the BBB to the extent that no further breakdowns would occur (8). The nonpharmacological treatments did not seem as commonly recommended as the pharmacological. This may return to a fear of the scientific community of the unknown, of things that cannot be
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