A New Era in Treating Multiple Sclerosis

Category: Multiple Sclerosis Published on Wednesday, 25 June 2008 Written by Yong Tsai, MD

Carolyn, the subject of our previous article, takes corticosteroids for her MS and other medications for associated symptoms, but recently, has experienced several flare-ups.  What can she do to decrease her flare-ups and to avoid further nerve damage?

Multiple sclerosis, like the Civil War, occurs when our body’s immune system turns our own T4 cells, a kind of important lymphocyte that protects us from infection and tumors, against our own brain and spinal cord tissue.  Even though they are from our own body (same country),  different genetic background (different ethnicity, beliefs and religion) sets them apart and triggers an incident like a virus (political agenda or policy change), thus creating autoimmune disease (civil war).

With MS, T4 cells, like our national guard, are called to active duty and equipped with cytokinases (orders, training, weapons, and transportation) in order to accomplish their mission: to cross the brain-blood-barrier (BBB), like the great divide, to gain entrance to the “battlefield” within the brain and spinal cord, and to take the offensive behind enemy line.

Prior to 1960, no special therapies were available for MS.  Then, in the 1960s, steroids became the foundation for treating MS until the late 1970s and early 1980s.  At this point, an increased understanding of the body’s immunologic changes associated with MS led to the pursuit of immunosuppressive agents such as those used to treat cancer or to prevent organ transplant rejection; Cyclophosphamide (Cytoxan), Azathioprine (Imuran), and Cyclosporin.  However, after several years, the excitement brought forth by these immunosuppressive agents gradually declined because of unsatisfactory results and substantial risk of toxicity.

In recent years, beta interferons (naturally occurring proteins) such as Avonex, Rebif, Betaseron and Glatiramer acetate (a mixture of amino acids), have been approved for treatment of MS. Essentially, these disease-modifying therapies actually work by adjusting our immune system and inflammatory process, by slowing down disease progress and by decreasing the recurrence and intensity of relapses. In some way, their effect is that of halting the order of calling the reservists to active duty and therefore decreasing the fighting in the battlefield.

Today, Natalizumab (Tysabri), a recently FDA approved monoclonal antibody, targets an adhesion molecule (transport vehicle), disabling these molecules so that the T4 cells cannot adhere to their “vehicle” used to cross the BBB “river”.  Therefore, the offensive T4 cells cannot gain access over enemy line.  This effect is what makes Tysabri, a monthly intravenous infusion, more effective than Glatiramer, a B interferon, in reducing relapses, increasing well being, and reducing further nerve and brain tissue damage.

The fact is that these new treatment options may have the ability to reverse even nerve damage, if treatment is started early, occurs in the early stages of relapsing-remitting MS in addition to being more effective in preventing frequent relapse and brain tissue damage.

Simultaneous use of multiple drugs to disrupt the several steps in the MS process may hold the key to future treatment.

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