Multiple Sclerosis Research Paper

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Multiple Sclerosis

Multiple sclerosis or MS refers to an autoimmune, chronic condition which impacts physical movement, function and sensation. The problem sets in following neuron insulation destruction (i.e., myelin sheath destruction) within an individual’s central nervous system (CNS) (Cengage Learning, 2013). Symptoms of the disorder start showing up at early adulthood, greatly impacting patients’ domestic, social, and professional lives. As the absence of myelin retards action potential conduct, the disorder is manifested as performance impairment, having a potential destructive influence on patient behavior. MS often entails a relatively progressive onset of behavioral deficiencies and neurological symptoms (Hoang & Shepherd, 2010).

Multiple Sclerosis and Nervous System

Chronic, advancing cognitive deterioration within multiple sclerosis has been ascribed to a neuro-pathological, neurodegenerative disease process (in other words, diffused brain atrophy and axonal destruction). Additionally, atrophy and white matter lesions are known to play a significant part in cognitive dysfunction among individuals diagnosed with MS; however, latest research proves grey matter lesions might be greatly influencing cognitive function (Rocca, Pravata & Valsasina, 2015).

Grey and white matter tissue inflammation within the central nervous system, on account of cytokine and focal immune cells’ infiltration, is initially responsible for MS-connected damage. A large number of research works indicate that CD4+ T cells or Th (T helper) cells intervene and their adaptive immune reactions triggered through T lymphocyte- APC (antigen presenting cell) interaction contribute greatly to MS onset and further development.
Pathogen-linked molecules join concurrently with toll-like APC receptors; further, release of interleukin IL-4, IL-23, IL-12, and other cytokines triggers differentiation of CD4+ T cells into Th1, Th17 or Th2 phenotypes that are capable of releasing special cytokines. Type II interferon or interferon gamma (IFN?) and TNF-? (tumor necrosis factor alpha) represent pro-inflammatory cytokines which are crucial to adaptive and intrinsic immunity. Th1 cells release such cytokines, which can promote inflammation through Th2 differentiation suppression. Th2 cells produce IL-13 and IL-4 (i.e., anti-inflammatory cytokines), both of which similarly affect immune cells. The former secretes matrix metalloproteinase, particularly at the time of allergic inflammation, while the latter decreases pathological inflammation through increasing M2/repair macrophages and alternatively activating pro-inflammatory M1 macrophages. Th17 – also a type of CD4+ T cell – induces various cytokines that promote inflammation (Ghasemi, Razavi & Nikzad, 2017).

Treatment of MS

Multiple sclerosis has no cure or disease prevention approach, as of the year 2016. Treatment differs based on….....

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References

Cengage Learning. (2013). Multiple Sclerosis. The Gale Encyclopedia of Nursing and Allied Health (3rd ed.).

Ghasemi, N., Razavi, R., & Nikzad, E. (2017). Multiple Sclerosis: Pathogenesis, symptoms, diagnoses and cell-based therapy. Cell J, 19(1), 1-10.

Hoang, P., Shepherd, R. (2010). Neurological rehabilitation: Optimizing motor performance (2nd ed.). Elsevier-Health Sciences Division: London.

Jock, M., Saunders, C., & Holland, N. (2012). Multiple Sclerosis (4th ed.). New York: Demos Health Publishing.

Rocca, M. A., Pravata, E., Valsasina, P. (2015). Hippocampal-DMN disconnectivity in MS is related to WM lesions and depression. Human Brain Mapping, 36(12), 5051–5063.
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