Although the exact underlying cause of the condition remains unknown, research has found links between the onset of MS and inflammation. Microglia are the main inflammatory cells of the CNS and can detect neural lesions and demyelination. Neuronal regions and white matter of the CNS are protected from the actions of the peripheral immune system due to the blood-brain barrier. Despite this anatomical division, the infiltration of T-cells into the CNS, due to signalled recruitment from microglia, can occur. This activation and migration of immune cells causes the release of inflammatory mediators such as cytokines, as well as further migration of other immune cells like macrophages and B-lymphocytes from the peripheral immune system. Antibodies cause tissue destruction and the release of intermediate products from macrophages elicit detrimental oxidative stress. Such products include nitrogen and reactive oxygen species, found to be linked to hypoxia through impaired mitochondrial functioning. In
creased inflammation of the brain ultimately can result in extensive demyelination of white matter, axonal degeneration, preventative axonal regeneration and neuronal cell death. It is yet to be determined whether the process of demyelination precedes or follows inflammation and neurodegeneration.
It has been found that MS is the most common neurological condition that young adults suffer from in the Western countries (Lassman et al). About 2,500,000 cases of MS have been reported globally, and prevalence rates in the England alone is around 64 per 00,000. Incidence rates tend to highlight that countries farther from the equator (both at a Northern or Southern distance) such as Scotland have higher MS rates. Geographical discrepancies in the epidemiology of MS imply that perhaps there are genetic factors as well as environmental effects that contribute to the susceptibility of tissue damage across individuals. Environmental factors include smoking, suggested to adversely hinder disease outcomes.