Abstract
Multiple sclerosis (MS) is a chronic debilitating inflammatory disease of unknown ethology targeting the central nervous system (CNS). MS has a polysymptomatic onset and is usually first diagnosed between the ages of 20–40 years. The pathology of the disease is characterized by immune mediated demyelination in the CNS. Although there is no clinical finding unique to MS, characteristic symptoms include sensory symptoms visual and motor impairment. No definitive trigger for the development of MS has been identified but large-scale population studies have described several epidemiological risk factors for the disease. This list is a confusing one including latitude, vitamin D (vitD) levels, genetics, infection with Epstein Barr Virus (EBV) and endogenous retrovirus (ERV) reactivation. This review will look at the evidence for each of these and the potential links between these disparate risk factors and the known molecular disease pathogenesis to describe potential hypotheses for the triggering of MS pathology.
Highlights
Multiple sclerosis (MS) pathology is characterized by multiple lesions within the central nervous system (CNS) [1]
Leukocyte migration can be inhibited by IFN-β and tissue inhibitor of metalloprotease 1 (TIMP-1) [22,23], suggesting that this process is regulated by immune mediators and requires metalloprotease
Environmental factors including viruses, where Epstein Barr Virus (EBV) infection and endogenous retrovirus reactivation have been connected to MS
Summary
MS pathology is characterized by multiple lesions within the CNS [1]. The pathogenesis of brain lesions remains largely unknown; neurodegeneration due to inflammation and immune reaction towards the brain cells is believed to play the central role. The presence of the brain plaques in the grey matter was demonstrated by Calabrese et al [4] These lesions could be detected early and correlate with the disease severity [5]. Leukocyte migration can be inhibited by IFN-β and tissue inhibitor of metalloprotease 1 (TIMP-1) [22,23], suggesting that this process is regulated by immune mediators and requires metalloprotease This assumption was further supported by Prat et al demonstrating that. Brain lesion localization and their number are related to clinical symptoms and clinical presentation, where the number of demyelination foci increases each time the patient experiences a clinical relapse [55] It appears that brain inflammation does continue in remission with the number of brain plaques increasing gradually during disease remission. When inflammation is localized in the optic nerve, signs such as blurry vision, ocular pain and visual loss are typically described [57]
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