Le système de santé britannique a franchi une étape décisive le 23 juillet 2026 en approuvant le remboursement de la fampridine pour les patients atteints de sclérose en plaques en Angleterre. Ce médicament, qualifié de « révolutionnaire » par les associations, est le premier spécifiquement autorisé pour améliorer la mobilité. Environ 5 000 personnes pourraient en bénéficier dès la première année.

Les chercheurs de Biogen et de l'Université de Pennsylvanie ont utilisé la transcriptomique spatiale combinée à l'analyse unicellulaire pour investiguer les mécanismes de démyélinisation et de remyélinisation dans le modèle à la cuprizone, largement utilisé pour étudier la sclérose en plaques. L'étude révèle une démyélinisation globale et une neuroinflammation au-delà du corps calleux, avec des variations régionales distinctes. Les oligodendroglia et la microglie émergent comme les principaux acteurs, présentant des signatures transcriptomiques spécifiques caractérisées par des gènes marqueurs tels qu'Arap2, Dock10 et ApoE. Durant la remyélinisation, les oligodendrocytes matures récupèrent largement leur phénotype initial, contrairement à la microglie qui conserve un profil associé à la démyélinisation. Les analyses d'appairage ligand-récepteur identifient les voies de facteurs de croissance et de phagocytose, mettant en évidence les interactions critiques entre oligodendroglia et microglie, ainsi qu'une nouvelle interaction entre oligodendrocytes matures et cellules précurseurs. Ces résultats améliorent la compréhension translationnelle du modèle et son pertinence pour les thérapies de remyélinisation.

Le document explore le rôle potentiel de la nociceptine/orphanin FQ (N/OFQ) dans la progression de la sclérose en plaques. Rédigé par Joseph Baker, cet article examine comment ce neuropeptide et son récepteur ORL-1 pourraient influencer les mécanismes pathologiques de cette maladie neuroinflammatore. La nociceptin/orphanin FQ est un peptide endogène impliqué dans la modulation de la douleur et de la neuroimmunité, ce qui en fait une cible thérapeutique intéressante pour la sclérose en plaques. L'article analyse les résultats de recherches précliniques et cliniques démontrant comment N/OFQ affecte l'activation microgliale, la neuroinflammation et la protection neuronale. Ces découvertes suggèrent que moduler le système nociceptinergique pourrait ouvrir de nouvelles voies thérapeutiques pour ralentir ou atténuer la progression de cette maladie chronique incurable. Ces résultats sont particulièrement importants pour développer des stratégies neuroprotectrices innovantes face à la sclérose en plaques.

Les Dispositifs d'Appui à la Coordination (DAC) constituent une infrastructure de santé territoriale visant à simplifier l'accès aux services pour les patients et professionnels confrontés à des parcours complexes. Chaque DAC fonctionne via un numéro d'appel unique par territoire, offrant un service gratuit accessible aux professionnels de santé, au secteur médico-social, aux patients et à leurs aidants. Composés d'équipes pluridisciplinaires regroupant médecins, infirmiers et travailleurs sociaux, les DAC informent, orientent et accompagnent les personnes en situation complexe, notamment celles présentant des polypathologies, des difficultés sociales ou psychologiques associées à des problèmes somatiques, ou souffrant d'isolement. Au-delà de l'appui individualisé, les DAC remplissent une mission d'animation territoriale en participant aux instances de coordination locale et en gérant des portails informationnels comme MAILLAGE, facilitant l'accès à l'actualité sanitaire et aux ressources locales. Ils orchestrent également des observatoires des parcours de santé pour identifier les ruptures de continuité et améliorer les pratiques professionnelles. À Paris et en Seine-et-Marne, plusieurs DAC opèrent sous différents porteurs, assurant une couverture territoriale optimale.

Le CHU de Toulouse a créé une Unité transversale d'éducation thérapeutique des patientes et patients (Utep) suite à une mission de l'ARS Occitanie. L'éducation thérapeutique des patientes et patients (ETP) est un processus éducatif continu intégré aux soins, destiné aux personnes atteintes de maladies chroniques. Elle favorise leur autonomie dans la gestion de leur condition en collaboration avec leur entourage et les soignants. L'Utep, composée de cinq membres à temps partiel, remplit quatre missions principales incluant la coordination de programmes d'ETP. Le CHU de Toulouse propose plusieurs programmes d'éducation thérapeutique adaptés à différentes pathologies, avec des informations disponibles sur les plateformes Oscar et monetp.fr. L'établissement offre également des formations diplômantes et non diplômantes aux professionnels de santé et aux patients souhaitant se développer dans le domaine de l'ETP, renforçant ainsi l'expertise collective en matière d'accompagnement thérapeutique.

Le NHS approuve pour la première fois en Angleterre le remboursement de la fampridine, un médicament révolutionnaire pour améliorer la mobilité des patients atteints de sclérose en plaques. Cette approbation, annoncée le 23 juillet 2026, met fin à une disparité territoriale au Royaume-Uni, le traitement étant déjà accessible au Pays de Galles, en Écosse et en Irlande du Nord. La fampridine agit comme un amplificateur de signal pour les nerfs endommagés, facilitant la transmission des messages électriques vers les muscles des jambes. Contrairement aux traitements modificateurs de la maladie, elle cible directement les symptômes invalidants liés à la mobilité chez les adultes présentant un score EDSS entre 4 et 7. Le protocole prévoit une phase de test de deux à quatre semaines pour identifier les répondeurs, avec un bénéfice démontré chez 43 % des participants aux essais cliniques. Environ 5 000 personnes pourraient être éligibles dès la première année. Cette approbation répond à un enjeu majeur : restaurer l'autonomie des patients en atténuant la fatigue extrême et les troubles de l'équilibre caractéristiques de la SEP.

Ocrelizumab is a newly approved disease-modifying therapy for multiple sclerosis that targets B cells in the immune system to prevent them from attacking the central nervous system. A comprehensive review examined its effectiveness across two MS types. In relapsing-remitting MS, ocrelizumab substantially reduced disease flare-ups and may substantially reduce symptom worsening compared to interferon beta-1a after 96 weeks, with similar rates of adverse effects. For primary progressive MS, ocrelizumab may reduce symptom progression versus placebo after 120 weeks of treatment, though it probably increases overall unwanted effects while showing little difference in serious adverse events. The research highlights ocrelizumab's potential to slow disease progression by blocking B cell-mediated inflammation and nerve damage. However, the review identifies a critical gap in evidence, concluding that more rigorously designed clinical studies are needed to fully establish ocrelizumab's long-term effectiveness and safety profile. These findings are significant for MS patients and healthcare providers evaluating treatment options, as they provide evidence-based guidance while underscoring the need for continued research to optimize therapeutic outcomes.

Tolebrrutinib, an experimental oral medication developed by Sanofi, represents a significant breakthrough for progressive multiple sclerosis patients who have long lacked effective therapeutic options. As a Bruton Tyrosine Kinase inhibitor (BTKi), tolebrrutinib targets BTK enzyme expressed by B lymphocytes and microglial cells—key immune cells responsible for brain inflammation and chronic lesion formation. Its distinctive advantage lies in its ability to cross the blood-brain barrier and simultaneously inhibit both cell types, effectively blocking the two major mechanisms driving demyelination: inflammatory cell infiltration and central nervous system immune activation. Notably, tolebrrutinib demonstrates real clinical impact on secondary progressive multiple sclerosis patients, a first for this patient population where relapses become rare but disability progresses irreversibly and increasingly. The European Medicines Agency's Committee for Medicinal Products for Human Use recently issued a favorable scientific opinion, paving the way for the final European Union marketing authorization decision. This development addresses an urgent unmet medical need affecting approximately half of patients with relapsing-remitting disease forms.

In 2016, Marseille's La Timone Hospital launched COMETE, a comprehensive educational toolkit designed to enhance therapeutic education for patients with multiple sclerosis. Developed to address recommendations from France's health authority, this pedagogical resource assists healthcare teams in fostering psychosocial competencies among patients. COMETE comprises structured activities, methodological guides, and card-based games targeting eight core competency areas: disease understanding, problem identification and resolution, self-image and life planning, emotional management, interpersonal relationships, social support systems, and self-confidence. The initiative distributed 280 copies throughout the PACA region's therapeutic education program coordinators. This resource represents a significant advancement in MS patient care by providing standardized, evidence-based tools that empower patients to better manage their condition while developing essential psychological and social skills necessary for improved treatment adherence and quality of life outcomes.

Stem cell therapies represent an emerging therapeutic approach for multiple sclerosis (MS), offering potential alternatives to conventional disease-modifying treatments. This comprehensive analysis examines the application of various stem cell types, including hematopoietic stem cells, mesenchymal stem cells, and neural progenitor cells, in MS management. The document reviews preclinical research, clinical trial data, and mechanistic insights into how stem cell transplantation may halt disease progression, reduce inflammation, and potentially promote remyelination of damaged nerve fibers. Key therapeutic mechanisms include immune system reconstitution, immunomodulation, and neuroprotection. The summary addresses both autologous stem cell transplantation protocols and allogeneic approaches, evaluating efficacy, safety profiles, and patient selection criteria. Evidence indicates that stem cell-based interventions show promise particularly in aggressive MS forms unresponsive to standard therapies. However, challenges remain regarding standardization of procedures, long-term safety monitoring, and cost-effectiveness. This field represents a significant paradigm shift in MS treatment, offering hope for patients with limited options while highlighting the need for rigorous clinical validation before broader implementation.

Multiple sclerosis research demonstrates that remyelination remains possible in adult human brains, particularly in relapsing-remitting forms where oligodendrocyte precursor cells (OPCs) can differentiate into mature oligodendrocytes to restore myelin sheaths around demyelinated nerve fibers. These newly formed sheaths, typically thinner than original coverings and identifiable as "shadow plaques" on imaging, may face renewed immune attack during disease relapses. Effective remyelination requires three essential components: available OPCs, stimuli to transform them into mature cells, and intact nerve fibers. A critical challenge is neuroprotection—preserving nerve fiber integrity during active inflammation and chronic degeneration, while recognizing that early remyelination provides the best neuroprotection. However, remyelination capacity varies significantly between patients and diminishes with age. Clinical measurement presents difficulties due to insufficient MRI specificity, and inhibitory factors at lesion sites further complicate the process. These interconnected challenges of neuroprotection and remyelination require coordinated therapeutic strategies to address MS progression effectively.

A new diploma program has been established to enhance the comprehensive care of multiple sclerosis patients by training healthcare professionals in developing personalized health pathways. Designed for medical and paramedical practitioners working in both hospital and community settings, the program emphasizes multidimensional patient assessment considering general, personal, professional, social, and psychological dimensions. The curriculum, integrated with the MS Resource and Coordination Center (CRC SEP) at Henri Mondor University Hospital and SINDEFI-SEP, covers fourteen core competency units delivered online, including MS neurology consultations, diagnostic follow-up, professional life management, disability compensation, therapeutic education, and care coordination. Graduates will possess the skills to construct and implement personalized health plans leveraging appropriate resources and stakeholders. The next cohort begins September 2026 through April 2027, with enrollment closing September 2026. Training fees are €1,330 plus €178 registration. Applications requiring CV, motivation letter, and diploma qualifications should be submitted to Fabienne Pelé at fabienne.pele@sindefi.org.

Multiple sclerosis is a chronic inflammatory neurological disorder affecting approximately 2.8 million people worldwide, where the immune system mistakenly attacks the protective sheath of nerve fibers in the central nervous system, disrupting communication between the brain and body. This causes diverse symptoms including coordination and balance disorders, movement difficulties, visual and cognitive impairments, often exacerbated by fatigue. The article introduces eye-tracking technology as a potential diagnostic tool, given that ocular movement circuits span multiple brain regions that may overlap with areas affected by MS. Current MS diagnosis relies on clinical evaluation, neurological examination, MRI imaging to visualize central nervous system lesions, and supplementary tests to exclude alternative causes, with clinicians adhering to revised McDonald criteria to standardize diagnosis. However, the article highlights a critical clinical concern: approximately 18 percent of MS diagnoses may be incorrect, with 50 percent of misdiagnosed patients retaining their false diagnosis for at least three years and 70 percent receiving disease-modifying treatments unnecessarily. The newsletter from neuroClues® emphasizes the importance of exploring eye-tracking technology to improve diagnostic accuracy and patient outcomes in MS management.

Multiple sclerosis treatment has undergone major transformations over the past three decades, evolving from initial platform molecules to high-efficacy therapies (HET), with disease-modifying treatments (DMT) now offering earlier, more targeted, and better-tolerated strategies. Understanding the mechanisms driving disability progression is essential for optimizing patient care. Three distinct mechanisms can lead to disability worsening: relapse-associated worsening (RAW), stemming from acute inflammation where controlling relapse risk is paramount; progression independent of relapse activity (PIRA), linked to compartmentalized central inflammation requiring Bruton tyrosine kinase inhibitors (BTKi), currently in development, for better targeting; and axonal degeneration resulting from the previous two phenomena. Three guiding principles have proven critical for reducing disability risk: treating as early as possible through timely diagnosis; prescribing high-efficacy therapy immediately; and maintaining treatment over the long term. This comprehensive approach reflects the evolution of MS management toward increasingly sophisticated and individualized therapeutic strategies designed to prevent progressive disability through early intervention and sustained disease control.

Multiple sclerosis is a chronic autoimmune inflammatory disease of the central nervous system characterized by distinct clinical presentations and evolving pathophysiology. Disability progression occurs through relapse-associated worsening, where repeated inflammatory episodes cause cumulative damage, and through progression independent of relapse activity, driven by compartmentalized microglial inflammation and secondary neurodegeneration. Prior to disease-modifying treatments, approximately half of patients required wheelchair assistance within fifteen to twenty years. Contemporary clinical outcomes have substantially improved through early diagnosis and initiation of high-efficacy treatments. The disease manifests in several distinct forms, including the most common relapsing-remitting presentation, characterized by focal relapses followed by complete or partial recovery within six months.

Stem cell therapy represents a revolutionary regenerative approach with variable success rates across different medical applications, from orthopedic pain relief to experimental neurological treatments. Recent scientific advances demonstrate significant progress in understanding treatment mechanisms and achieving evidence-based practices. Research reveals promising outcomes including improved functional recovery in neurological disorders and orthopedic injuries, alongside enhanced tissue regeneration. Simultaneously, studies have identified methods to mitigate adverse effects such as tumorigenesis and immune-mediated complications. These developments have refined safety protocols and patient selection criteria, enabling more personalized treatment approaches. Success rates in stem cell therapy are measured by patients achieving desired outcomes such as symptom reduction, disease remission, or improved quality of life, though efficacy and safety profiles continue to evolve as the field matures.

T- and B-cell depletion has emerged as a pivotal immunotherapeutic approach for managing autoimmune diseases by selectively eliminating autoreactive lymphocytes. T-cell depletion interrupts pathogenic activation cascades and aberrant immune interactions, while B-cell depletion suppresses antigen presentation and autoantibody generation. Modern depletion technologies, including monoclonal antibodies, engineered biologics, bispecific agents, and cellular therapies, deliver enhanced specificity with minimal off-target immunosuppression. Understanding lymphocyte reconstitution and compensatory immune mechanisms has refined therapeutic optimization, enabling precision-based interventions that achieve sustained disease control while maintaining targeted immunomodulation.

OFSEP operates an integrated digital infrastructure supporting multiple sclerosis research and clinical management across France. The EDMUS software serves as a computerized medical record system enabling neurologists to document and analyze patient data efficiently. The Shanoir platform provides secure web-based access for structuring, managing, and sharing neuroimaging data, with automated tools facilitating anonymized MRI transfers from hospital systems. TumoroteK manages biological samples across participating biobanks, creating a virtual centralized repository while maintaining anonymized data integrity. Together, these interconnected open-source systems enable comprehensive data collection, standardization, and collaborative research while ensuring patient privacy and clinical utility.

This 2026 epigenetic lexicon compiles 45 fundamental concepts spanning from DNA methylation to sirtuines, including TADs, X-inactivation, and epigenetic aging. Epigenetics, positioned at the intersection of genetics and cellular biology, examines mechanisms that modulate gene expression without altering DNA sequences. These mechanisms, such as methylation and histone modifications, function as molecular switches, influencing organismal development, environmental adaptation, and intergenerational trait transmission. Each term is explained accessibly yet precisely, accompanied by concrete examples and health implications. The lexicon serves as an essential reference guide for students, researchers, and life sciences enthusiasts seeking to understand how molecular processes like acetylation and RNA interference regulate gene activity and contribute to conditions ranging from cancer to neurodegenerative diseases, offering insights into cutting-edge epigenetic discoveries.

Une entreprise de biotechnologie basée à Boston a lancé le premier essai clinique chez l’homme d’une thérapie de reprogrammation cellulaire, marquant ainsi une étape importante dans la lutte contre le vieillissement cellulaire. Ce traitement, baptisé ER-100, cible la perte de vision liée à l’âge et le glaucome en reprogrammant les cellules vieillissantes pour leur redonner un état plus jeune grâce à une restauration épigénétique. Développée par Life Biosciences, société cofondée par le généticien David Sinclair, cette thérapie utilise un virus modifié pour introduire trois gènes soigneusement sélectionnés — OCT4, SOX2 et KLF4 — qui réinitialisent les horloges cellulaires. L’œil a été stratégiquement choisi comme premier terrain d’essai en raison de son isolement relatif par rapport au reste du corps, ce qui minimise les effets indésirables systémiques potentiels. Cette approche s’appuie sur les travaux pionniers du lauréat du prix Nobel Shinya Yamanaka et sur des études antérieures menées dans des laboratoires de Harvard, qui ont démontré une régénération neuronale et une restauration de la vision réussies chez des souris atteintes de glaucome.