[{"data":1,"prerenderedAt":-1},["ShallowReactive",2],{"doc-seo-411298-105":3,"detail-sidebar-cat-0-en-105":81,"doc-detail-411298-en":130},{"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","controversies-in-multiple-sclerosis-remyelination-therapies-are-achievable-in-clinical-practiceyes","Controversies in Multiple Sclerosis - Remyelination therapies are achievable in clinical practice—Yes","","High-efficacy disease-modifying therapies have reduced relapses and new lesions in multiple sclerosis, yet many patients still face persistent disability from incomplete recovery and progressive functional decline that current treatments cannot reverse demyelination. Chronic demyelination drives impairment of signal conduction and increases vulnerability to axonal injury and neurodegeneration, making remyelination a leading neuroprotective strategy. The article evaluates whether remyelination is neuroprotective, feasible and measurable in people with MS, and clinically meaningful, arguing the answer is likely yes when appropriate patients, biology, and outcomes are selected.",{"@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/controversies-in-multiple-sclerosis-remyelination-therapies-are-achievable-in-clinical-practiceyes/411298/",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/controversies-in-multiple-sclerosis-remyelination-therapies-are-achievable-in-clinical-practiceyes/411298.png","ImageObject",300,407,{"name":42,"@type":43},"Pentious","Person",{"url":19,"name":45,"@type":46},"DocShare","Organization","application/pdf","2026-10-30","2026-09-28",true,{"@type":52,"interactionType":53,"userInteractionCount":55},"InteractionCounter",{"@type":54},"ViewAction",6,{"@type":57,"mainEntity":58},"FAQPage",[59,65,69],{"name":60,"@type":61,"acceptedAnswer":62},"Why is remyelination considered important in multiple sclerosis?","Question",{"text":63,"@type":64},"Because chronic demyelination contributes to disability by disrupting efficient signal transduction and leaving axons vulnerable to injury and neurodegeneration. Therapies that promote remyelination are presented as a promising neuroprotection approach.","Answer",{"name":66,"@type":61,"acceptedAnswer":67},"What evidence suggests remyelination is neuroprotective?",{"text":68,"@type":64},"Animal models indicate that impaired remyelination leads to more axonal injury and functional decline, while accelerating remyelination improves both. Human data are described as consistent, including axonal injury assessments in tissue and measurable neuroprotection markers such as serum NfL and VEP latency changes.",{"name":70,"@type":61,"acceptedAnswer":71},"How is remyelination measured and shown to be achievable in clinical practice?",{"text":72,"@type":64},"The article discusses measurable outcomes in remyelinating candidates, emphasizing VEP latency improvements and MRI metrics like myelin water fraction. It highlights the ReBUILD trial as proof of concept and notes ongoing/anticipated results from the CCMR-Two trial.","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},411298,1790841172,{"code":4,"msg":82,"data":83},"success",[84,88,92,96,101,105,109,114,119,122,126],{"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":55,"doc_module":4,"doc_module_name":25,"category_name":102,"show_sort_weight":103,"slug":104},"Technology",50,"technology",{"id":106,"doc_module":4,"doc_module_name":25,"category_name":29,"show_sort_weight":107,"slug":108},7,40,"healthcare",{"id":110,"doc_module":4,"doc_module_name":25,"category_name":111,"show_sort_weight":112,"slug":113},8,"Research & Report",30,"research-report",{"id":115,"doc_module":4,"doc_module_name":25,"category_name":116,"show_sort_weight":117,"slug":118},9,"Religion & Spirituality",20,"religion-spirituality",{"id":117,"doc_module":4,"doc_module_name":25,"category_name":120,"show_sort_weight":117,"slug":121},"World Cup","world-cup",{"id":123,"doc_module":4,"doc_module_name":25,"category_name":124,"show_sort_weight":123,"slug":125},10,"Lifestyle","lifestyle",{"id":127,"doc_module":4,"doc_module_name":25,"category_name":128,"show_sort_weight":97,"slug":129},19,"General","general",{"code":4,"msg":82,"data":131},{"doc_id":79,"user_id":132,"nickname":42,"user_avatar":133,"doc_module":4,"category_id":106,"category_name":29,"doc_title":10,"doc_description":12,"doc_content":134,"file_id":135,"file_url":136,"file_type":137,"file_size":138,"view_count":55,"is_deleted":4,"is_public":22,"is_downloadable":22,"audit_status":22,"page_count":30,"language":139,"language_code":8,"site_id":7,"html_lang":8,"table_of_contents":140,"faqs":141,"seo_title":142,"seo_description":12,"update_tm":143,"read_time":110,"preview_page_count":4},1374404730887,"https://ap-avatar.wpscdn.com/davatar_6f874abed73319feea01a86fa6f0fab8","MULTIPLE SCLEROSIS JOURNAL  \nMSJ  \nControversies in Multiple Sclerosis  \nRemyelination therapies are achievable in clinical practice—Yes  \nLeah Zuroff, Christian Cordano and Ari J Green  \nMultiple Sclerosis Journal 2026, Vol. 32(1) 54–56 DOI: 10. 1177/ 13524585251396272 © The Author(s), 2025.  \nArticle reuse guidelines: [sagepub.com/journals](sagepub.com/journals)permissions  \nThe advent of high-efficacy disease-modifying therapies (DMTs) has transformed multiple sclerosis (MS), dramatically reducing relapses and lesion formation and improving quality of life for many patients. Yet, important challenges remain. Many people with multiple sclerosis (pwMS) continue to live with disability, driven by incomplete recovery from inflammatory injury and insidious functional decline across all phases of disease. Both forms of disability remain inadequately addressed by current therapies. In fact, none are able to promote recovery from either new or remote demyelinating injury.  \nChronic demyelination contributes to disability by impairing efficient signal transduction and leaving axons metabolically vulnerable to injury and neurodegeneration.1 Thus, therapies that promote remyelination are among the most promising approaches for neuroprotection in pwMS.  \nWe strongly believe that remyelination is possible. However, for remyelination to be impactful, we must ask: (1) Is remyelination neuroprotective? (2) Is it feasible and measurable in pwMS? and (3) Is it clinically meaningful? We argue the answer to all three is likely yes—provided we identify the right patients, biology, and outcomes.  \nIs remyelination neuroprotective?  \nAnimal models strongly suggest that remyelination is neuron- and axon-protective. In multiple inflammatory and genetic models of demyelination, impaired remyelination leads to more pronounced axonal injury and functional decline,2 while accelerating remyelination significantly improves both measures.3,4  \nHuman data from pwMS corroborate this relationship. In MS autopsy tissue, acutely or chronically demyelinated lesions exhibit high degrees of axonal injury, while “shadow plaques” (remyelinated or  \nincompletely demyelinated lesions) contain levels of axonal injury comparable to control white matter.5  \nMeanwhile, in vivo, serum neurofilament light chain (NfL) can be used to measure axonal damage. In two independent trials of remyelinating candidates, clemastine and bexarotene, treatment was associated with reduced serum NfL levels, suggesting that therapeutic remyelination provides measurable neuroprotection.6,7 In addition, following optic neuritis, visual evoked potential (VEP) latency—a measure of myelin integrity within the visual pathway8—was inversely associated with the extent of retinal nerve fiber layer degeneration.9,10  \nIs promoting remyelination feasible and measurable in pwMS?  \nEndogenous remyelination likely occurs in pwMS, albeit variably and incompletely. Potential reasons for remyelination failure include impaired oligodendrocyte precursor cell (OPC) recruitment, differentiation, and survival. Drug development has mainly targeted OPC differentiation, though other mechanisms may hold promise.  \nThe phase II ReBUILD trial established proof of concept that remyelination is achievable. In this randomized, placebo-controlled, cross-over trial of 50 pwMS with chronic demyelinating optic neuropathy, clemastine fumarate (M1 muscarinic receptor antagonist) significantly improved VEP latency versus placebo by 1.7 msec/eye.11 Delayed-treatment analyses showed improved low contrast letter acuity, and exploratory analyses demonstrated increased myelin water fraction (a quantitative magnetic resonance imaging [MRI] measure of myelin) in the corpus callosum.12 The CCMR-Two trial, which studied the combination of clemastine fumarate and metformin, was also recently reported to have met its primary endpoint of improved VEP latency in MS patients  \nCorrespondence to:  \nAJ Green  \nDivision of Neuroimmunology and Gl","cbCaif6eQFp1x8Qy","https://ap.wps.com/l/cbCaif6eQFp1x8Qy","pdf",574903,"English","# Remyelination as a neuroprotective strategy\n# Evidence that remyelination is neuroprotective\n# Feasibility and measurability in people with multiple sclerosis\n## ReBUILD trial results\n## CCMR-Two trial results\n## Other early remyelination program outcomes","[{\"question\":\"Why is remyelination considered important in multiple sclerosis?\",\"answer\":\"Because chronic demyelination contributes to disability by disrupting efficient signal transduction and leaving axons vulnerable to injury and neurodegeneration. Therapies that promote remyelination are presented as a promising neuroprotection approach.\"},{\"question\":\"What evidence suggests remyelination is neuroprotective?\",\"answer\":\"Animal models indicate that impaired remyelination leads to more axonal injury and functional decline, while accelerating remyelination improves both. Human data are described as consistent, including axonal injury assessments in tissue and measurable neuroprotection markers such as serum NfL and VEP latency changes.\"},{\"question\":\"How is remyelination measured and shown to be achievable in clinical practice?\",\"answer\":\"The article discusses measurable outcomes in remyelinating candidates, emphasizing VEP latency improvements and MRI metrics like myelin water fraction. It highlights the ReBUILD trial as proof of concept and notes ongoing/anticipated results from the CCMR-Two trial.\"}]","Controversies in Multiple Sclerosis - Remyelination therapies are achievable in clinical practice—Yes | PDF",1790588114]