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Multiple Sclerosis is a disease which primarily affects the central nervous system. This chronic and inflammatory disease is often accompanied by numerous symptoms such as physical changes including sensation problems, visual problems and muscle weakness (Dangond 2005). There are also other psychological disorders that accompany it such as depression, coordination and speech problems and cognitive impairment (Altmann 2005). In certain severe cases, it has also been cited to cause disability or severe impaired mobility (Altmann 2005).

The problem with multiple sclerosis is that while its form has been identified and symptom narrowed down, there is still no agreement within the scientific community as to what really causes multiple sclerosis. There are certain scientists who maintain that multiple sclerosis is the result of an attack by an individual’s immune system on the nervous system (Altmann 2005). This theory on multiple sclerosis being an autoimmune disease has been rejected by certain scientists, however, arguing that multiple sclerosis is a metabolically dependent neurodegenerative disease (Chaudhuri 2004).

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This disagreement is seen as a boon of sorts because it has led to the development of many new therapies for multiple sclerosis. Currently, there has been research involving a new class of molecules called the sphingosine-1-phosphate receptor modulators which have been shown to slow down the effects of multiple sclerosis (Kappos et al. 2006). This is still in the phase II part of its research, however, with the third phase set to begin within the year (Kappos et al. 2006). Other current therapies that are currently being developed involve the simple remedy of taking vitamin D especially for women (Munger 2004).

A recent study has shown that women who took vitamin D supplements were 40% less likely to develop MS than women who did not take supplements. This is still debated as there is no delineation between the exact effects of Vitamin D as differentiated from the protective effect of Vitamin E (Munger 2004). The most recent journal published in February of 2007 by Canadian scientists has shown that a certain hormone called prolactin has been found to ease and even reverse the effects of multiple sclerosis on the body.

It was observed in the pregnant rats used in the test that the hormone protects the myelin, which coats the brain and spinal cord, from the damage associated with multiple sclerosis. This came from the increased levels of prolactin in the pregnant rats during the research. There is still a lot of testing that needs to be done at this stage, however, and it has not been approved as a cure for multiple sclerosis in humans at the present time (Zabad 2007).

Other current researches being funded by the National Multiple Sclerosis Society include research on effect of the CD24 molecule that is said to enhance the EAE development through the co-stimulation of T cells (Liu 2007). Another research project addresses the need to effectively regulate and control the regulatory responses of diseases such as multiple sclerosis by controlling the tissue inflammation around the affected area. This study assumes that multiple sclerosis as an autoimmune disease can only be controlled by first reducing the tissue inflammation (Korn 2007).

While there is definitely no consensus yet as to the exact cause of multiple sclerosis, the disagreement among the different scientific groups has indeed helped improve the study of this field. The numerous researches, aside from those mentioned here, have all helped at bringing the scientific and medical world much closer to a possible cure or antidote for multiple sclerosis. References: Altmann D (2005). “Evaluating the evidence for multiple sclerosis as an autoimmune disease”. Arch. Neurol. 62 (4): 688; author reply 688-9. PMID 15824275

Chaudhuri A, Behan P (2004). “Multiple sclerosis is not an autoimmune disease”. Arch. Neurol. 61 (10): 1610–2. PMID 15477520 Dangond, F. Multiple sclerosis. eMedicine Neurology. Updated 2005 Apr 25 Korn T, Reddy J, Gao W, Bettelli E, Awasthi A, Petersen TR, Backstrom BT, Sobel RA, Wucherpfennig KW, Strom TB, Oukka M, Kuchroo VK. Myelin-specific regulatory T cells accumulate in the CNS but fail to control autoimmune inflammation. Nat Med. 2007 Apr;13(4):423-31. Epub 2007 Mar 25. Liu JQ, Carl JW Jr, Joshi PS, Raychaudhury A, Pu XA, Shi FD, Bai XF.

J Immunol CD24 on the Resident Cells of the Central Nervous System Enhances Experimental Autoimmune Encephalomyelitis . 2007 May 15;178(10):6227-35. Ludwig Kappos, M. D. , Jack Antel, M. D. , Giancarlo Comi, M. D. , Xavier Montalban, M. D. , Paul O’Connor, M. D. , Chris H. Polman, M. D. , Tomas Haas, Ph. D. , Alexander A. Korn, Ph. D. , Goeril Karlsson, Ph. D. , Ernst W. Radue, M. D. , for the FTY720 D2201 Study Group. NEJM,Volume 355:1124-1140 Munger KL, Zhang SM, O’Reilly E, Hernan MA, Olek MJ, Willett WC, Ascherio A. Vitamin D intake and incidence of multiple sclerosis. Neurology. 2004 Jan 13;62(1):60-5. PMID 14718698

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