[{"data":1,"prerenderedAt":-1},["ShallowReactive",2],{"doc-seo-458851-105":3,"detail-sidebar-cat-0-en-105":81,"doc-detail-458851-en":131},{"code":4,"msg":5,"data":6},0,"ok",{"site_id":7,"language":8,"slug":9,"title":10,"keywords":11,"description":12,"schema_data":13,"social_meta":74,"head_meta":76,"extra_data":78,"updated_unix":80},105,"en","ageing-and-remyelination-failure-in-people-with-multiple-sclerosis","Ageing and remyelination failure in people with multiple sclerosis","","Ageing and remyelination failure in people with multiple sclerosis is examined through a review of pathological, imaging, and clinical evidence linking older age to reduced endogenous remyelination. The analysis addresses why measuring remyelination in humans is challenging and evaluates whether an age cutoff exists. Findings indicate diminished remyelination capacity with advancing age, though results can be inconsistent and the precise ageing contribution remains unclear. Lesion location may influence the age effect. With evidence suggesting ageing biology could be modifiable, the review supports targeting ageing pathways to improve remyelination therapeutically.",{"@graph":14,"@context":73},[15,34,56],{"@type":16,"itemListElement":17},"BreadcrumbList",[18,23,27,31],{"item":19,"name":20,"@type":21,"position":22},"https://docshare.wps.com","Home","ListItem",1,{"item":24,"name":25,"@type":21,"position":26},"https://docshare.wps.com/document/","Document",2,{"item":28,"name":29,"@type":21,"position":30},"https://docshare.wps.com/document/healthcare/","Healthcare",3,{"item":32,"name":10,"@type":21,"position":33},"https://docshare.wps.com/document/ageing-and-remyelination-failure-in-people-with-multiple-sclerosis/458851/",4,{"url":32,"name":10,"@type":35,"image":36,"author":41,"headline":10,"publisher":44,"fileFormat":47,"inLanguage":8,"description":12,"dateModified":48,"datePublished":49,"encodingFormat":47,"isAccessibleForFree":50,"interactionStatistic":51},"DigitalDocument",{"url":37,"@type":38,"width":39,"height":40},"https://docshare.wps.com/thumbnails/ageing-and-remyelination-failure-in-people-with-multiple-sclerosis/458851.png","ImageObject",300,407,{"name":42,"@type":43},"Danger Angel","Person",{"url":19,"name":45,"@type":46},"DocShare","Organization","application/pdf","2026-11-04","2026-09-30",true,{"@type":52,"interactionType":53,"userInteractionCount":55},"InteractionCounter",{"@type":54},"ViewAction",12,{"@type":57,"mainEntity":58},"FAQPage",[59,65,69],{"name":60,"@type":61,"acceptedAnswer":62},"What is the main therapeutic strategy discussed for multiple sclerosis disability progression?","Question",{"text":63,"@type":64},"Enhancing endogenous remyelination is described as a leading strategy to delay, prevent, or reverse disability progression in multiple sclerosis by improving the repair of myelin.","Answer",{"name":66,"@type":61,"acceptedAnswer":67},"What does preclinical evidence suggest about ageing and remyelination?",{"text":68,"@type":64},"In aged rodent models, differentiation of oligodendrocyte precursor cells into mature myelinating oligodendrocytes becomes rate-limiting, and aged OPCs fail to differentiate even with pro-differentiation factors.",{"name":70,"@type":61,"acceptedAnswer":71},"Is there an age cutoff beyond which remyelination is impossible in multiple sclerosis?",{"text":72,"@type":64},"The review indicates there does not appear to be a strict age cutoff, because pathological data support remyelination occurring to some extent across all ages.","https://schema.org",{"og:url":32,"og:type":75,"og:title":10,"og:site_name":45,"og:description":12},"article",{"robots":77,"canonical":32},"index,follow",{"doc_id":79,"site_id":7},458851,1791079347,{"code":4,"msg":82,"data":83},"success",[84,88,92,96,101,106,110,115,120,123,127],{"id":22,"doc_module":4,"doc_module_name":25,"category_name":85,"show_sort_weight":86,"slug":87},"Story & Novel",90,"story-novel",{"id":26,"doc_module":4,"doc_module_name":25,"category_name":89,"show_sort_weight":90,"slug":91},"Literature",80,"literature",{"id":33,"doc_module":4,"doc_module_name":25,"category_name":93,"show_sort_weight":94,"slug":95},"Exam",70,"exam",{"id":97,"doc_module":4,"doc_module_name":25,"category_name":98,"show_sort_weight":99,"slug":100},5,"Comic",60,"comic",{"id":102,"doc_module":4,"doc_module_name":25,"category_name":103,"show_sort_weight":104,"slug":105},6,"Technology",50,"technology",{"id":107,"doc_module":4,"doc_module_name":25,"category_name":29,"show_sort_weight":108,"slug":109},7,40,"healthcare",{"id":111,"doc_module":4,"doc_module_name":25,"category_name":112,"show_sort_weight":113,"slug":114},8,"Research & Report",30,"research-report",{"id":116,"doc_module":4,"doc_module_name":25,"category_name":117,"show_sort_weight":118,"slug":119},9,"Religion & Spirituality",20,"religion-spirituality",{"id":118,"doc_module":4,"doc_module_name":25,"category_name":121,"show_sort_weight":118,"slug":122},"World Cup","world-cup",{"id":124,"doc_module":4,"doc_module_name":25,"category_name":125,"show_sort_weight":124,"slug":126},10,"Lifestyle","lifestyle",{"id":128,"doc_module":4,"doc_module_name":25,"category_name":129,"show_sort_weight":97,"slug":130},19,"General","general",{"code":4,"msg":82,"data":132},{"doc_id":79,"user_id":133,"nickname":42,"user_avatar":134,"doc_module":4,"category_id":107,"category_name":29,"doc_title":10,"doc_description":12,"doc_content":135,"file_id":136,"file_url":137,"file_type":138,"file_size":139,"view_count":55,"is_deleted":4,"is_public":22,"is_downloadable":22,"audit_status":22,"page_count":140,"language":141,"language_code":8,"site_id":7,"html_lang":8,"table_of_contents":142,"faqs":143,"seo_title":144,"seo_description":12,"update_tm":145,"read_time":146,"preview_page_count":4},962090769052,"https://ap-avatar.wpscdn.com/davatar_9964176cb1d06d4a9deccf72a44ae3dc","[https://doi.org/10.1093/brain/awaf373](https://doi.org/10.1093/brain/awaf373) BRAIN 2026: 149; 48–58 | 48  \nAgeing and remyelination failure in people with multiple sclerosis  \nTrisha Mukherjee,1 Christopher E. McMurran,1 Jonathon Holland,1  \nCyrus Daruwalla,1 Gioia Riboni-Verri,1 J. William L. Brown,1 Robin J. M. Franklin,2 Alasdair Coles1 and Nick G. Cunniffe1  \nOne of the most promising strategies to delay, prevent, or reverse disability progression in multiple sclerosis is enhancing endogenous remyelination. While preclinical research has established a strong connection between ageing and remyelination failure, evidence for this same link in people with multiple sclerosis remains less secure. As clinical trials for remyelinating therapies progress, clarifying this relationship is essential. A deeper understanding could guide the selection of therapeutic candidates, refine patient selection, and optimize the timing of treatment delivery. In this review, we describe the available evidence that has investigated the impact of age on remyelination in people with multiple sclerosis. We categorize these into pathological, imaging and clinical studies. We explore the challenges in measuring remyelination inhumans and determine the implications for the connection between remyelination and age. Current evidence suggests that there is reduced capacity for remyelination with advancing age in people with multiple sclerosis. However, these findings are at times inconsistent, and the precise contribution of ageing to remyelination failure is unclear. There does not appear to be an age cut-off beyond which remyelination is not possible, as there are pathological data supporting remyelination occurring, to some extent, across all ages. Interestingly, the impact of age may vary by lesion location. Further targeted research, specifically exploring the relationship between ageing and remyelination, is needed. With emerging evidence that ageing processes might be malleable, we conclude that targeting the biology of ageing might also be an important strategy to therapeutically enhance remyelination.  \n1 Department of Clinical Neurosciences, University of Cambridge, Cambridge CB2 0QQ, UK  \n2 Altos Labs—Cambridge Institute of Science, Granta Park, Cambridge CB21 6GQ, UK  \nCorrespondence to: Christopher E. McMurran  \nDepartment of Clinical Neurosciences, University of Cambridge Cambridge Biomedical Campus, Box 157, Level 5 Addenbrookes Hospital, Hills Road, Cambridge CB2 0QQ, UK  \nE-mail: [cem73@cam.ac.uk](cem73@cam.ac.uk)  \nKeywords: myelin; oligodendrocyte precursor cell; magnetization transfer ratio; g-ratio; visual evoked potentials; biological ageing  \nIntroduction  \nPromoting endogenous remyelination decreases the vulnerability of demyelinated axons to irreversible degeneration and is therefore a leading strategy to treat disability progression in people with multiple sclerosis (MS) .1 Remyelination is primarily achieved through a choreographed process of activation, migration, proliferation and  \ndifferentiation of oligodendrocyte progenitor cells (OPCs) into newly-formed myelinating oligodendrocytes.2 In experimental models, each stage of this regenerative process becomes less efficient with age (reviewed by Neumann et al.3) . Understanding whether ageing similarly impacts remyelination capacity in people with MS is critical for the successful development of remyelinating therapies.  \nReceived April 22, 2025. Revised August 29, 2025. Accepted September 03, 2025. Advance access publication October 6, 2025 © The Author(s) 2025. Published by Oxford University Press on behalf of the Guarantors of Brain.  \nThis is an Open Access article distributed under the terms of the Creative Commons Attribution License ([https://creativecommons.org/licenses/by/4.0/](https://creativecommons.org/licenses/by/4.0/)), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.  \nAge and remyelin","cbCaip0cUq9MBk3P","https://ap.wps.com/l/cbCaip0cUq9MBk3P","pdf",383441,11,"English","# Introduction\n## Remyelination as a therapeutic strategy in multiple sclerosis\n## Age effects in experimental models\n## Age-related deficits and potential reversibility\n# Age-dependent remyelination variation in people with multiple sclerosis","[{\"question\":\"What is the main therapeutic strategy discussed for multiple sclerosis disability progression?\",\"answer\":\"Enhancing endogenous remyelination is described as a leading strategy to delay, prevent, or reverse disability progression in multiple sclerosis by improving the repair of myelin.\"},{\"question\":\"What does preclinical evidence suggest about ageing and remyelination?\",\"answer\":\"In aged rodent models, differentiation of oligodendrocyte precursor cells into mature myelinating oligodendrocytes becomes rate-limiting, and aged OPCs fail to differentiate even with pro-differentiation factors.\"},{\"question\":\"Is there an age cutoff beyond which remyelination is impossible in multiple sclerosis?\",\"answer\":\"The review indicates there does not appear to be a strict age cutoff, because pathological data support remyelination occurring to some extent across all ages.\"}]","Ageing and remyelination failure in people with multiple sclerosis | PDF",1790754607,28]