Abstract
In multiple sclerosis, conduction block in demyelinated axons underlies early neurological symptoms, whereas axonal transection is believed to be responsible for more permanent later deficits. Approved treatments for the disease are immunoregulatory and reduce the rate of lesion formation and clinical exacerbation, but are only partially effective in preventing the onset of disability. Remyelination is a term for the re-generation of the nerve's myelin sheath and is a subject of active medical research. Remyelination capacity varies from patient to patient or even from lesion to lesion in one and the same patient. Efforts to understand the causes for remyelination failure have prompted research into the biology of remyelination and the complex molecular factors that regulate remyelination.
In the current review article we address challenges of remyelination research with a special focus on histo-pathological studies using brain biopsy and autopsy material. We summarize our current knowledge about extent of remyelination in multiple sclerosis patients and its relation to disease duration, lesion type, inflammation, affected brain region and gender. Furthermore we will address which step(s) of the oligodendrocyte maturation program is impaired and, thus, could be a feasible target for therapeutic interventions. Specifically mentioned will be the distribution of oligodendrocyte progenitor cells in demyelinated multiple sclerosis plaques and therapeutic approaches which aim to boost intrinsic properties of progenitor cells or to supply progenitors by cell transplantation approaches. This comprehensive overview is complemented by recent findings suggesting that U.S. Food and Drug Administration-approved treatment options, such as FTY720 (Gilenya®) or glatiramer acetate (Copaxone®) might boost myelin repair.
Keywords: Cuprizone, multiple sclerosis, oligodendrocytes, regeneration, remyelination, repair.
CNS & Neurological Disorders - Drug Targets
Title:Endogeneous Remyelination: Findings in Human Studies
Volume: 11 Issue: 5
Author(s): Markus Kipp, Marion Victor, Gianvito Martino and Robin J.M. Franklin
Affiliation:
Keywords: Cuprizone, multiple sclerosis, oligodendrocytes, regeneration, remyelination, repair.
Abstract: In multiple sclerosis, conduction block in demyelinated axons underlies early neurological symptoms, whereas axonal transection is believed to be responsible for more permanent later deficits. Approved treatments for the disease are immunoregulatory and reduce the rate of lesion formation and clinical exacerbation, but are only partially effective in preventing the onset of disability. Remyelination is a term for the re-generation of the nerve's myelin sheath and is a subject of active medical research. Remyelination capacity varies from patient to patient or even from lesion to lesion in one and the same patient. Efforts to understand the causes for remyelination failure have prompted research into the biology of remyelination and the complex molecular factors that regulate remyelination.
In the current review article we address challenges of remyelination research with a special focus on histo-pathological studies using brain biopsy and autopsy material. We summarize our current knowledge about extent of remyelination in multiple sclerosis patients and its relation to disease duration, lesion type, inflammation, affected brain region and gender. Furthermore we will address which step(s) of the oligodendrocyte maturation program is impaired and, thus, could be a feasible target for therapeutic interventions. Specifically mentioned will be the distribution of oligodendrocyte progenitor cells in demyelinated multiple sclerosis plaques and therapeutic approaches which aim to boost intrinsic properties of progenitor cells or to supply progenitors by cell transplantation approaches. This comprehensive overview is complemented by recent findings suggesting that U.S. Food and Drug Administration-approved treatment options, such as FTY720 (Gilenya®) or glatiramer acetate (Copaxone®) might boost myelin repair.
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Cite this article as:
Kipp Markus, Victor Marion, Martino Gianvito and J.M. Franklin Robin, Endogeneous Remyelination: Findings in Human Studies, CNS & Neurological Disorders - Drug Targets 2012; 11 (5) . https://dx.doi.org/10.2174/187152712801661257
DOI https://dx.doi.org/10.2174/187152712801661257 |
Print ISSN 1871-5273 |
Publisher Name Bentham Science Publisher |
Online ISSN 1996-3181 |
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