Overview Of Multiple Sclerosis

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This essay intends to compare two diseases, Multiple sclerosis (MS) and Crohn’s disease (CD), in order to evaluate the statement “apart from anatomical location, pathological processes in the CNS and the rest of the body are the same.” Both MS and CD belong to a group of diseases which share common inflammatory pathways, called immune-mediated inflammatory diseases (IMIDs) (Kuek, A., et al. 2007). An imbalance in the cytokines within these conditions are central to the pathogenesis of the diseases (Hur, S. J., et al., 2012). CD is characterised by a relapsing inflammatory process which manifests within the gut and is mediated by T cells (Kuek, A., et al. 2007). The cause of CD is unknown, but a number of factors are thought to contribute to the manifestation of CD, including: genetic; environmental; bacterial; immunological equilibrium (Selby, W., 2000). Like CD, the causes of MS are largely unknown, however it is believed that genetic, environmental and immunological components play a pivotal role in the development of MS (Huynh, J. L., Casaccia, P., 2013). MS is an inflammatory disease in which the myelin sheath surrounding the axons of nerve cells are destroyed through immune processes (Wingerchuk, D. M., Lucchinetti, C. F., Noseworthy, J. H., 2001). Genome wide association studies have linked inflammatory bowel disease with associated autoimmune diseases, such as MS. This was found from epidemiological studies on a molecular level showing shared susceptibility loci and was then able to explain ethnic differences (Bernstein, C. N., Wajda, A. & Blanchard, J. F., 2005). Genome wide association studies, as well as computerised meta-analysis, have located and established 71 susceptibility loci for Crohn’s disease on 17 chromosomes ... ... middle of paper ... ...etion of perforin, which has a cytotoxic effect upon CD4+ T cells and this leads to their subsequent inactivation (Loma, I. & Heyman, R., 2011). Furthermore, CD8+ cells kill glial cells which results in the exposure of the axons, as well as transecting the axons and thus promoting vascular permeability and activation of oligodendrocyte death (Wingerchuk, D. M., Lucchinetti, C. F., Noseworthy, J. H., 2001). As can be seen from the disease mechanisms from both CD and MS, the key player within these mechanisms is the development of inflammation. Although the anatomical site of inflammation differs, MS being within the CNS and CD in the GI tract, CD4+ cells feature heavily within the pathogenesis of both diseases. Over expression of the CD4+ cells results in an inflammatory cascade which results in chronic inflammation and subsequent tissue damage in both CD and MS.
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