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Therapeutic Advances and Biomarkers in Multiple Sclerosis
1Department of Neurology, Cantonal Hospital of Biel/Bienne, Biel/Bienne, Switzerland.
Introduction:
High-efficacy Disease-Modifying Therapies (DMTs) have transformed relapse control in multiple sclerosis, yet Progression Independent of Relapse Activity (PIRA) persists. This review aims to synthesize contemporary therapeutic advances and clarify how emerging biomarkers assess treatment efficacy.
Methods:
This narrative review includes randomized trials, prospective cohorts, open-label extensions, and major regulatory/congress communications through August 2025.
Results:
Anti-CD20 monoclonal antibodies consolidate first-line status in active disease and consistently reduce serum Neurofilament Light (sNfL). Anti-CD40L antibodies lower new gadoliniumenhancing lesions and produce sustained sNfL decreases in phase 2. Extended-interval natalizumab and Sphingosine-1-Phosphate (S1P) receptor modulators reduce relapses and MRI activity. CNSpenetrant Bruton's Tyrosine Kinase (BTK) inhibitors target compartmentalized inflammation, with mixed late-phase results. Immune-reconstitution strategies provide durable disease control with rapid, sustained sNfL suppression, while Glial Fibrillary Acidic Protein (GFAP) changes less, aligning with progression biology. EBV-directed approaches show early feasibility, with biomarkeranchored approaches; CD19 Chimeric Antigen Receptor T-cell (CAR-T) therapy remains investigational. Remyelination/neurorepair candidates show signal on visual evoked potentials and myelinsensitive MRI.
Discussion:
Anti-CD20 antibodies are foundational in RRMS and PPMS; S1P modulators remain effective in Relapsing Remitting Multiple Sclerosis (RRMS) and relapsing Secondary Progressive Multiple Sclerosis (SPMS). Immune-reconstitution strategies can provide durable control, while anti-CD40L, BTK inhibitors, EBV-directed and CD19 CAR-T, and remyelination approaches are promising but require definitive trials. Across therapies, sNfL generally decreases, whereas GFAP and smouldering-lesion MRI biomarkers often change more slowly.
Conclusion:
Contemporary care reliably controls inflammatory activity, but mitigating PIRA remains the key unmet need. Routine sNfL monitoring, complemented by GFAP and advanced imaging, may refine response assessment and risk stratification for progression.
