Myelin Recovery in Multiple Sclerosis: The Challenge of Remyelination
Multiple sclerosis (MS) is the most common demyelinating and an autoimmune disease of the central nervous system characterized by immune-mediated myelin and axonal damage, and chronic axonal loss attributable to the absence of myelin sheaths. T cell subsets (Th1, Th2, Th17, CD8+, NKT, CD4+CD25+ T re...
| Main Authors: | , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
MDPI AG
2013-08-01
|
| Series: | Brain Sciences |
| Subjects: | |
| Online Access: | http://www.mdpi.com/2076-3425/3/3/1282 |
| _version_ | 1828230114209431552 |
|---|---|
| author | Edward L. Hogan Ewa Kurowska Naren L. Banik Maria Podbielska |
| author_facet | Edward L. Hogan Ewa Kurowska Naren L. Banik Maria Podbielska |
| author_sort | Edward L. Hogan |
| collection | DOAJ |
| description | Multiple sclerosis (MS) is the most common demyelinating and an autoimmune disease of the central nervous system characterized by immune-mediated myelin and axonal damage, and chronic axonal loss attributable to the absence of myelin sheaths. T cell subsets (Th1, Th2, Th17, CD8+, NKT, CD4+CD25+ T regulatory cells) and B cells are involved in this disorder, thus new MS therapies seek damage prevention by resetting multiple components of the immune system. The currently approved therapies are immunoregulatory and reduce the number and rate of lesion formation but are only partially effective. This review summarizes current understanding of the processes at issue: myelination, demyelination and remyelination—with emphasis upon myelin composition/ architecture and oligodendrocyte maturation and differentiation. The translational options target oligodendrocyte protection and myelin repair in animal models and assess their relevance in human. Remyelination may be enhanced by signals that promote myelin formation and repair. The crucial question of why remyelination fails is approached is several ways by examining the role in remyelination of available MS medications and avenues being actively pursued to promote remyelination including: (i) cytokine-based immune-intervention (targeting calpain inhibition), (ii) antigen-based immunomodulation (targeting glycolipid-reactive iNKT cells and sphingoid mediated inflammation) and (iii) recombinant monoclonal antibodies-induced remyelination. |
| first_indexed | 2024-04-12T18:43:34Z |
| format | Article |
| id | doaj.art-86638f90a95e4f5983fe22d91e2b3ec8 |
| institution | Directory Open Access Journal |
| issn | 2076-3425 |
| language | English |
| last_indexed | 2024-04-12T18:43:34Z |
| publishDate | 2013-08-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Brain Sciences |
| spelling | doaj.art-86638f90a95e4f5983fe22d91e2b3ec82022-12-22T03:20:41ZengMDPI AGBrain Sciences2076-34252013-08-01331282132410.3390/brainsci3031282Myelin Recovery in Multiple Sclerosis: The Challenge of RemyelinationEdward L. HoganEwa KurowskaNaren L. BanikMaria PodbielskaMultiple sclerosis (MS) is the most common demyelinating and an autoimmune disease of the central nervous system characterized by immune-mediated myelin and axonal damage, and chronic axonal loss attributable to the absence of myelin sheaths. T cell subsets (Th1, Th2, Th17, CD8+, NKT, CD4+CD25+ T regulatory cells) and B cells are involved in this disorder, thus new MS therapies seek damage prevention by resetting multiple components of the immune system. The currently approved therapies are immunoregulatory and reduce the number and rate of lesion formation but are only partially effective. This review summarizes current understanding of the processes at issue: myelination, demyelination and remyelination—with emphasis upon myelin composition/ architecture and oligodendrocyte maturation and differentiation. The translational options target oligodendrocyte protection and myelin repair in animal models and assess their relevance in human. Remyelination may be enhanced by signals that promote myelin formation and repair. The crucial question of why remyelination fails is approached is several ways by examining the role in remyelination of available MS medications and avenues being actively pursued to promote remyelination including: (i) cytokine-based immune-intervention (targeting calpain inhibition), (ii) antigen-based immunomodulation (targeting glycolipid-reactive iNKT cells and sphingoid mediated inflammation) and (iii) recombinant monoclonal antibodies-induced remyelination.http://www.mdpi.com/2076-3425/3/3/1282calpaincentral nervous systemdemyelinationfingolimodglycolipidslipidsmultiple sclerosismyelinmyelinationNKT cellsoligodendrocytesremyelinationT cells |
| spellingShingle | Edward L. Hogan Ewa Kurowska Naren L. Banik Maria Podbielska Myelin Recovery in Multiple Sclerosis: The Challenge of Remyelination Brain Sciences calpain central nervous system demyelination fingolimod glycolipids lipids multiple sclerosis myelin myelination NKT cells oligodendrocytes remyelination T cells |
| title | Myelin Recovery in Multiple Sclerosis: The Challenge of Remyelination |
| title_full | Myelin Recovery in Multiple Sclerosis: The Challenge of Remyelination |
| title_fullStr | Myelin Recovery in Multiple Sclerosis: The Challenge of Remyelination |
| title_full_unstemmed | Myelin Recovery in Multiple Sclerosis: The Challenge of Remyelination |
| title_short | Myelin Recovery in Multiple Sclerosis: The Challenge of Remyelination |
| title_sort | myelin recovery in multiple sclerosis the challenge of remyelination |
| topic | calpain central nervous system demyelination fingolimod glycolipids lipids multiple sclerosis myelin myelination NKT cells oligodendrocytes remyelination T cells |
| url | http://www.mdpi.com/2076-3425/3/3/1282 |
| work_keys_str_mv | AT edwardlhogan myelinrecoveryinmultiplesclerosisthechallengeofremyelination AT ewakurowska myelinrecoveryinmultiplesclerosisthechallengeofremyelination AT narenlbanik myelinrecoveryinmultiplesclerosisthechallengeofremyelination AT mariapodbielska myelinrecoveryinmultiplesclerosisthechallengeofremyelination |