Multiple sclerosis pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Pathophysiology
Multiple sclerosis is a disease of central nervous system and it’s known to be multifactorial. There are both inflammation and degeneration in the course of the disease but as its progress, degeneration becomes more prominent.[1] Whatever the trigger is, it will lead to acquired immune response followed by inflammatory reactions. This reactions lead to secretion of cytokines in CNS parenchyma and activation of resident microglia. Microglia cells activate astrocytes to release more inflammatory cytokines leading to recruitment and infiltration of circulatory leukocytes.[2][3][4]
References
- ↑ Fiorini A, Koudriavtseva T, Bucaj E, Coccia R, Foppoli C, Giorgi A, Schininà ME, Di Domenico F, De Marco F, Perluigi M (2013). "Involvement of oxidative stress in occurrence of relapses in multiple sclerosis: the spectrum of oxidatively modified serum proteins detected by proteomics and redox proteomics analysis". PLoS ONE. 8 (6): e65184. doi:10.1371/journal.pone.0065184. PMC 3676399. PMID 23762311.
- ↑ John GR, Lee SC, Song X, Rivieccio M, Brosnan CF (2005). "IL-1-regulated responses in astrocytes: relevance to injury and recovery". Glia. 49 (2): 161–76. doi:10.1002/glia.20109. PMID 15472994.
- ↑ Kawakami N, Nägerl UV, Odoardi F, Bonhoeffer T, Wekerle H, Flügel A (2005). "Live imaging of effector cell trafficking and autoantigen recognition within the unfolding autoimmune encephalomyelitis lesion". J. Exp. Med. 201 (11): 1805–14. doi:10.1084/jem.20050011. PMC 2213265. PMID 15939794.
- ↑ Sofroniew MV (2015). "Astrocyte barriers to neurotoxic inflammation". Nat. Rev. Neurosci. 16 (5): 249–63. doi:10.1038/nrn3898. PMC 5253239. PMID 25891508.