New insights into remyelination failure in multiple sclerosis: implications for glial cell transplantation
This review considers aspects of remyelination that require further clarification if successful strategies are to be devised to enhance remyelination in multiple sclerosis (MS). We speculate, based on our understanding of the rate with which oligodendrocyte progenitor cells (OPCs) repopulate OPC-dep...
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Veröffentlicht in: | Multiple sclerosis 2002-08, Vol.8 (4), p.271-277 |
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description | This review considers aspects of remyelination that require further clarification if successful strategies are to be devised to enhance remyelination in multiple sclerosis (MS). We speculate, based on our understanding of the rate with which oligodendrocyte progenitor cells (OPCs) repopulate OPC-depleted tissue in adult rats, that OPC depletion during the demyelination process could explain why remyelination fails in MS. We show that loss of OPCs in the context of large areas of demyelination would have serious consequences for remyelination as the rates of colonization of tissue by adult OPCs would lead to a situation where the cellular events associated with demyelination become uncoupled from the interaction of OPCs with demyelinated axons. Experimental studies indicate that transplanted neonatal OPCs would be able to repopulate large areas of demyelination with much greater efficiency than endogenous OPCs. This suggests that cell transplantation will have considerable potential to achieve remyelination in situations where the endogenous repair process is failing due to concurrent death of oligodendrocytes and OPCs. However, we suggest that for this approach to be effective, it will be critical that the environment is permissive for remyelination. |
doi_str_mv | 10.1191/1352458502ms842oa |
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We speculate, based on our understanding of the rate with which oligodendrocyte progenitor cells (OPCs) repopulate OPC-depleted tissue in adult rats, that OPC depletion during the demyelination process could explain why remyelination fails in MS. We show that loss of OPCs in the context of large areas of demyelination would have serious consequences for remyelination as the rates of colonization of tissue by adult OPCs would lead to a situation where the cellular events associated with demyelination become uncoupled from the interaction of OPCs with demyelinated axons. Experimental studies indicate that transplanted neonatal OPCs would be able to repopulate large areas of demyelination with much greater efficiency than endogenous OPCs. This suggests that cell transplantation will have considerable potential to achieve remyelination in situations where the endogenous repair process is failing due to concurrent death of oligodendrocytes and OPCs. However, we suggest that for this approach to be effective, it will be critical that the environment is permissive for remyelination.</description><identifier>ISSN: 1352-4585</identifier><identifier>EISSN: 1477-0970</identifier><identifier>DOI: 10.1191/1352458502ms842oa</identifier><identifier>PMID: 12166495</identifier><identifier>CODEN: MUSCFZ</identifier><language>eng</language><publisher>Thousand Oaks, CA: SAGE Publications</publisher><subject>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy ; Animals ; Applied cell therapy and gene therapy ; Biological and medical sciences ; Demyelinating Diseases - pathology ; Demyelinating Diseases - surgery ; Humans ; Medical sciences ; Multiple Sclerosis - pathology ; Multiple Sclerosis - surgery ; Nerve Regeneration ; Oligodendroglia - transplantation ; Stem Cell Transplantation ; Transfusions. Complications. Transfusion reactions. 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We speculate, based on our understanding of the rate with which oligodendrocyte progenitor cells (OPCs) repopulate OPC-depleted tissue in adult rats, that OPC depletion during the demyelination process could explain why remyelination fails in MS. We show that loss of OPCs in the context of large areas of demyelination would have serious consequences for remyelination as the rates of colonization of tissue by adult OPCs would lead to a situation where the cellular events associated with demyelination become uncoupled from the interaction of OPCs with demyelinated axons. Experimental studies indicate that transplanted neonatal OPCs would be able to repopulate large areas of demyelination with much greater efficiency than endogenous OPCs. This suggests that cell transplantation will have considerable potential to achieve remyelination in situations where the endogenous repair process is failing due to concurrent death of oligodendrocytes and OPCs. However, we suggest that for this approach to be effective, it will be critical that the environment is permissive for remyelination.</description><subject>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</subject><subject>Animals</subject><subject>Applied cell therapy and gene therapy</subject><subject>Biological and medical sciences</subject><subject>Demyelinating Diseases - pathology</subject><subject>Demyelinating Diseases - surgery</subject><subject>Humans</subject><subject>Medical sciences</subject><subject>Multiple Sclerosis - pathology</subject><subject>Multiple Sclerosis - surgery</subject><subject>Nerve Regeneration</subject><subject>Oligodendroglia - transplantation</subject><subject>Stem Cell Transplantation</subject><subject>Transfusions. Complications. Transfusion reactions. 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Intensive care medicine. Transfusions. Cell therapy and gene therapy</topic><topic>Animals</topic><topic>Applied cell therapy and gene therapy</topic><topic>Biological and medical sciences</topic><topic>Demyelinating Diseases - pathology</topic><topic>Demyelinating Diseases - surgery</topic><topic>Humans</topic><topic>Medical sciences</topic><topic>Multiple Sclerosis - pathology</topic><topic>Multiple Sclerosis - surgery</topic><topic>Nerve Regeneration</topic><topic>Oligodendroglia - transplantation</topic><topic>Stem Cell Transplantation</topic><topic>Transfusions. Complications. Transfusion reactions. Cell and gene therapy</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chari, D M</creatorcontrib><creatorcontrib>Blakemore, W F</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Consumer Health Database (Alumni Edition)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Consumer Health Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>Multiple sclerosis</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chari, D M</au><au>Blakemore, W F</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>New insights into remyelination failure in multiple sclerosis: implications for glial cell transplantation</atitle><jtitle>Multiple sclerosis</jtitle><addtitle>Mult Scler</addtitle><date>2002-08-01</date><risdate>2002</risdate><volume>8</volume><issue>4</issue><spage>271</spage><epage>277</epage><pages>271-277</pages><issn>1352-4585</issn><eissn>1477-0970</eissn><coden>MUSCFZ</coden><abstract>This review considers aspects of remyelination that require further clarification if successful strategies are to be devised to enhance remyelination in multiple sclerosis (MS). We speculate, based on our understanding of the rate with which oligodendrocyte progenitor cells (OPCs) repopulate OPC-depleted tissue in adult rats, that OPC depletion during the demyelination process could explain why remyelination fails in MS. We show that loss of OPCs in the context of large areas of demyelination would have serious consequences for remyelination as the rates of colonization of tissue by adult OPCs would lead to a situation where the cellular events associated with demyelination become uncoupled from the interaction of OPCs with demyelinated axons. Experimental studies indicate that transplanted neonatal OPCs would be able to repopulate large areas of demyelination with much greater efficiency than endogenous OPCs. This suggests that cell transplantation will have considerable potential to achieve remyelination in situations where the endogenous repair process is failing due to concurrent death of oligodendrocytes and OPCs. However, we suggest that for this approach to be effective, it will be critical that the environment is permissive for remyelination.</abstract><cop>Thousand Oaks, CA</cop><pub>SAGE Publications</pub><pmid>12166495</pmid><doi>10.1191/1352458502ms842oa</doi><tpages>7</tpages></addata></record> |
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subjects | Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy Animals Applied cell therapy and gene therapy Biological and medical sciences Demyelinating Diseases - pathology Demyelinating Diseases - surgery Humans Medical sciences Multiple Sclerosis - pathology Multiple Sclerosis - surgery Nerve Regeneration Oligodendroglia - transplantation Stem Cell Transplantation Transfusions. Complications. Transfusion reactions. Cell and gene therapy |
title | New insights into remyelination failure in multiple sclerosis: implications for glial cell transplantation |
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