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The nervous and immune systems have many interactions that dictate overall body health. The nervous system is under constant monitoring from both the [[adaptive]] and [[innate immune system]]. Throughout development and adult life, the immune system detects and responds to changes in [[cell identity]] and neural connectivity.<ref>Bailey, S.L., Carpentier, P.A., McMahon, E.J., Begolka, W.S., Miller, S.D., 2006. Innate and adaptive immune responses of the central nervous system. [[Critical Reviews in Immunology]]. 26, 149–188.</ref> Deregulation of both adaptive and acquired immune responses, impairment of crosstalk between these two systems, as well as alterations in the deployment of innate immune mechanisms can predispose the [[central nervous system]] (CNS) to autoimmunity and neurodegeneration.<ref>{{cite journal |author1=Hauser S.L. |author2=Oksenberg J.R. | year = 2006 | title = The neurobiology of multiple sclerosis: genes, inflammation, and neurodegeneration | url = | journal = Neuron | volume = 52 | issue = | pages = 61–76 | doi=10.1016/j.neuron.2006.09.011}}</ref> Other evidence has shown that development and deployment of the innate and acquired immune systems in response to stressors on functional integrity of cellular and systemic level and the evolution of autoimmunity are mediated by [[epigenetic mechanisms]].<ref>{{cite journal | author = Sawalha A.H. | year = 2008 | title = Epigenetics and T-cell immunity | url = | journal = Autoimmunity | volume = 41 | issue = | pages = 245–252 | doi=10.1080/08916930802024145}}</ref> Autoimmunity has been increasingly linked to targeted deregulation of epigenetic mechanisms, and therefore, use of epigenetic therapeutic agents may help reverse complex pathogenic processes.<ref>Gray, S.G., Dangond, F., 2006. Rationale for the use of histone [[deacetylase]] inhibitors as a dual therapeutic modality in multiple sclerosis. Epigenetics 1, 67–75.</ref> [[Multiple sclerosis]] (MS) is one type of neuroimmunological disorder that affects many people. MS features CNS inflammation, immune-mediated demyelination and neurodegeneration, and may represent an emerging class of epigenetic disorders.<ref>{{cite journal | author = Brooks W.H. | year = 2005 | title = Autoimmune disorders result from loss of epigenetic control following chromosome damage | url = | journal = [[Medical Hypotheses]] | volume = 64 | issue = | pages = 590–598 | doi=10.1016/j.mehy.2004.08.005 | pmid=15617874}}</ref>{{ums|date=November 2017}}
Myalgic Encephalomyelitis (also known as [[Chronic fatigue syndrome]]), is a multi-system disease that causes dysfunction of neurological, immune, endocrine and energy-metabolism systems. Though many patients show neuroimmunological degeneration, the correct roots of ME/CFS are unknown. Symptoms of ME/CFS include significantly lowered ability to participate in regular activities, stand or sit straight, inability to talk, sleep problems, excessive sensitivity to light, sound or touch and/or thinking and memory problems (defective cognitive functioning). Other common symptoms are muscle or joint pain, [[sore throat]] or [[night sweats]]. There is no treatment but symptoms may be treated. Patients that are sensitive to [[mold]] may show improvement in symptoms having moved to drier areas. Some patients in general have less severe ME, whereas others may be bedridden for life.<ref>{{cite web |title=WHAT IS ME? |url=https://www.meaction.net/about/what-is-me/ |website=MEAction |accessdate=21 August 2018}}</ref>
==Major themes of research==
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