Changes in deoxyribonucleic acid methylation contribute to the pathophysiology of multiple sclerosis
dc.contributor.author
dc.date.accessioned
2022-02-23T12:22:01Z
dc.date.available
2022-02-23T12:22:01Z
dc.date.issued
2019-11-12
dc.identifier.uri
dc.description.abstract
Multiple sclerosis (MS) is an autoimmune disease of the central nervous system characterized by loss of coordination, weakness, dysfunctions in bladder capacity, bowel movement, and cognitive impairment. Thus, the disease leads to a significant socioeconomic burden. In the pathophysiology of the disease, both genetic and environmental risk factors are involved. Gene x environment interaction is modulated by epigenetic mechanisms. Epigenetics refers to a sophisticated system that regulates gene expression with no changes in the DNA sequence. The most studied epigenetic mechanism is the DNA methylation. In this review, we summarize the data available from the current literature by grouping sets of differentially methylated genes in distinct biological categories: the immune system including innate and adaptive response, the DNA damage, and the central nervous system
dc.description.sponsorship
This review was funded by the Deutsche
Forschungsgemeinschaft to Dr. Jordi Tomas Roig (ref. TO
977/1-1) and the University of Girona to Mrs Naiara Celarain
Sanz (ref. IFUdG2017)
dc.format.mimetype
application/pdf
dc.language.iso
eng
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Reproducció digital del document publicat a: https://doi.org/10.3389/fgene.2019.01138
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Frontiers in Genetics, 2019, vol. 10, art.núm. 1138
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Articles publicats (IdIBGi)
dc.rights
Reconeixement 4.0 Internacional
dc.rights.uri
dc.source
Celarain, Naiara Tomàs Roig, Jordi 2019 Changes in deoxyribonucleic acid methylation contribute to the pathophysiology of multiple sclerosis Frontiers In Genetics
dc.subject
dc.title
Changes in deoxyribonucleic acid methylation contribute to the pathophysiology of multiple sclerosis
dc.type
info:eu-repo/semantics/article
dc.rights.accessRights
info:eu-repo/semantics/openAccess
dc.type.version
info:eu-repo/semantics/publishedVersion
dc.identifier.doi
dc.identifier.idgrec
034876
dc.type.peerreviewed
peer-reviewed
dc.identifier.eissn
1664-8021