Multiple sclerosis pathophysiology: Difference between revisions
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== Pathophysiology == | == 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.<ref name="pmid23762311">{{cite journal |vauthors=Fiorini A, Koudriavtseva T, Bucaj E, Coccia R, Foppoli C, Giorgi A, Schininà ME, Di Domenico F, De Marco F, Perluigi M |title=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 |journal=PLoS ONE |volume=8 |issue=6 |pages=e65184 |year=2013 |pmid=23762311 |pmc=3676399 |doi=10.1371/journal.pone.0065184 |url=}}</ref> Whatever the trigger is, it will lead to acquired [[immune response]] followed by [[Inflammation|inflammatory]] reactions. This reactions lead to secretion of [[cytokines]] in [[CNS]] [[parenchyma]] and activation of resident [[microglia]]. [[Microglia]] cells activate [[astrocytes]] to release more [[Inflammation|inflammatory]] [[cytokines]] leading to recruitment and [[Infiltration (medical)|infiltration]] of circulatory [[leukocytes]].<ref name="pmid15472994">{{cite journal |vauthors=John GR, Lee SC, Song X, Rivieccio M, Brosnan CF |title=IL-1-regulated responses in astrocytes: relevance to injury and recovery |journal=Glia |volume=49 |issue=2 |pages=161–76 |year=2005 |pmid=15472994 |doi=10.1002/glia.20109 |url=}}</ref><ref name="pmid15939794">{{cite journal |vauthors=Kawakami N, Nägerl UV, Odoardi F, Bonhoeffer T, Wekerle H, Flügel A |title=Live imaging of effector cell trafficking and autoantigen recognition within the unfolding autoimmune encephalomyelitis lesion |journal=J. Exp. Med. |volume=201 |issue=11 |pages=1805–14 |year=2005 |pmid=15939794 |pmc=2213265 |doi=10.1084/jem.20050011 |url=}}</ref><ref name="pmid25891508">{{cite journal |vauthors=Sofroniew MV |title=Astrocyte barriers to neurotoxic inflammation |journal=Nat. Rev. Neurosci. |volume=16 |issue=5 |pages=249–63 |year=2015 |pmid=25891508 |pmc=5253239 |doi=10.1038/nrn3898 |url=}}</ref> This burst events cause destruction of myelin and CNS tissue and releasing more auto antigens including myelin oligodendrocyte glycoprotein (MOG), myelin basic protein (MBP), proteolipid protein (PLP).<ref name="pmid22933080">{{cite journal |vauthors=McCarthy DP, Richards MH, Miller SD |title=Mouse models of multiple sclerosis: experimental autoimmune encephalomyelitis and Theiler's virus-induced demyelinating disease |journal=Methods Mol. Biol. |volume=900 |issue= |pages=381–401 |year=2012 |pmid=22933080 |pmc=3583382 |doi=10.1007/978-1-60761-720-4_19 |url=}}</ref> | 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.<ref name="pmid23762311">{{cite journal |vauthors=Fiorini A, Koudriavtseva T, Bucaj E, Coccia R, Foppoli C, Giorgi A, Schininà ME, Di Domenico F, De Marco F, Perluigi M |title=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 |journal=PLoS ONE |volume=8 |issue=6 |pages=e65184 |year=2013 |pmid=23762311 |pmc=3676399 |doi=10.1371/journal.pone.0065184 |url=}}</ref> There are variety of different [[cell]]<nowiki/>s participating in [[MS]] [[pathophysiology]]. Whatever the trigger is, it will lead to acquired [[immune response]] followed by [[Inflammation|inflammatory]] reactions. This reactions lead to secretion of [[cytokines]] in [[CNS]] [[parenchyma]] and activation of resident [[microglia]]. [[Microglia]] cells activate [[astrocytes]] to release more [[Inflammation|inflammatory]] [[cytokines]] leading to recruitment and [[Infiltration (medical)|infiltration]] of circulatory [[leukocytes]].<ref name="pmid15472994">{{cite journal |vauthors=John GR, Lee SC, Song X, Rivieccio M, Brosnan CF |title=IL-1-regulated responses in astrocytes: relevance to injury and recovery |journal=Glia |volume=49 |issue=2 |pages=161–76 |year=2005 |pmid=15472994 |doi=10.1002/glia.20109 |url=}}</ref><ref name="pmid15939794">{{cite journal |vauthors=Kawakami N, Nägerl UV, Odoardi F, Bonhoeffer T, Wekerle H, Flügel A |title=Live imaging of effector cell trafficking and autoantigen recognition within the unfolding autoimmune encephalomyelitis lesion |journal=J. Exp. Med. |volume=201 |issue=11 |pages=1805–14 |year=2005 |pmid=15939794 |pmc=2213265 |doi=10.1084/jem.20050011 |url=}}</ref><ref name="pmid25891508">{{cite journal |vauthors=Sofroniew MV |title=Astrocyte barriers to neurotoxic inflammation |journal=Nat. Rev. Neurosci. |volume=16 |issue=5 |pages=249–63 |year=2015 |pmid=25891508 |pmc=5253239 |doi=10.1038/nrn3898 |url=}}</ref> This burst events cause destruction of [[myelin sheath]] and [[CNS]] tissue and releasing more auto antigens including [[myelin oligodendrocyte glycoprotein]] (MOG), [[myelin basic protein]] (MBP), [[proteolipid protein]] (PLP).<ref name="pmid22933080">{{cite journal |vauthors=McCarthy DP, Richards MH, Miller SD |title=Mouse models of multiple sclerosis: experimental autoimmune encephalomyelitis and Theiler's virus-induced demyelinating disease |journal=Methods Mol. Biol. |volume=900 |issue= |pages=381–401 |year=2012 |pmid=22933080 |pmc=3583382 |doi=10.1007/978-1-60761-720-4_19 |url=}}</ref> | ||
==References== | ==References== | ||
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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] There are variety of different cells participating in MS pathophysiology. 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] This burst events cause destruction of myelin sheath and CNS tissue and releasing more auto antigens including myelin oligodendrocyte glycoprotein (MOG), myelin basic protein (MBP), proteolipid protein (PLP).[5]
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.
- ↑ McCarthy DP, Richards MH, Miller SD (2012). "Mouse models of multiple sclerosis: experimental autoimmune encephalomyelitis and Theiler's virus-induced demyelinating disease". Methods Mol. Biol. 900: 381–401. doi:10.1007/978-1-60761-720-4_19. PMC 3583382. PMID 22933080.