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Multiple sclerose (MS) es un autoimmun maladia neurodegenerative affectante le copertura del cellulas nervose del cerebro e medulla spinal.

Multiple sclerose
instantia de: designated intractable/rare disease[*], classe de maladias[*], symptom or sign[*]
subclasse de: maladia demyelinisante[*], demyelinating disease of central nervous system[*], autoimmune disease of central nervous system[*], maladia


Commons: Multiple sclerosis

Signos e symptomas

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HLA region del chromosoma 6: cambios in iste area augmenta le probabilitate de disveloppar un MS.

MS non es considerate como un maladia hereditari ma plure genetic variationes augmenta le risco de disveloppar lo.[1]

Genes ligate con MS include human leukocyte antigen (HLA) systema — un gruppo de genes sul chromosoma 6 qui servi como major histocompatibilitate complexo (MHC).[2] Le cambios in HLA region pote alsi esser implicate in the disveloppamento de altere autoimmun disordines, como diabete de typo I o lupo erythematose systemic.[3] Le association le plus consistente concerna allelos DR15 e DQ6 del MHC.[2] Foras HLA locos, al minus 200 variantes pote augmentar un pauc le probabilitate de MS.[4]

Un genetic variante locate inter genes DYSF e ZNF638 permitterea un progression plus rapide del maladia.[5][6]

Referentias

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  1. "Genetics of multiple sclerosis" (February 2004). The Lancet. Neurology 3 (2): 104–10. doi:10.1016/S1474-4422(03)00663-X. PMID 14747002. 
  2. 2,0 2,1 "Multiple sclerosis" (October 2008). Lancet 372 (9648): 1502–1517. doi:10.1016/S0140-6736(08)61620-7. PMID 18970977. 
  3. "Revealing the genetic basis of multiple sclerosis: are we there yet?" (June 2011). Current Opinion in Genetics & Development 21 (3): 317–24. doi:10.1016/j.gde.2010.12.006. PMID 21247752. 
  4. International Multiple Sclerosis Genetics Consortium (2019). "Multiple sclerosis genomic map implicates peripheral immune cells and microglia in susceptibility.". Science 365 (6460). doi:10.1126/science.aav7188. PMID 31604244. 
  5. https://neurosciencenews.com/genetics-progressive-ms-23546/
  6. doi:10.1038/s41586-023-06250-x