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Multiple Sclerosis: From Molecular Pathology to Novel Therapeutic Approaches

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".

Deadline for manuscript submissions: 30 June 2025 | Viewed by 60

Special Issue Editor


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Guest Editor
1. HUN-REN-SZTE Neuroscience Research Group, Hungarian Research Network, University of Szeged (HUN-REN-SZTE), Danube Neuroscience Research Laboratory, Tisza Lajos krt. 113, H-6725 Szeged, Hungary
2. Department of Neurology, Albert Szent-Györgyi Medical School, University of Szeged, Semmelweis u. 6, H-6725 Szeged, Hungary
Interests: multiple sclerosis; neurodegeneration; smouldering lesion; molecular pathology; novel therapies; kynurenines
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Special Issue Information

Dear Colleagues,

Multiple sclerosis (MS) is a chronic disease characterised by inflammation, extensive primary demyelination, and progressive neurodegenerative processes. Long-term disability in MS is largely independent of relapses (progression independent of relapse activity, PIRA) and correlates well with brain atrophy detected by MRI images. Smouldering lesions show a low-grade chronic inflammation characterised by chronic axonal damage and concurrent demyelination and are further characterised by a gradual increase in size towards the normal-appearing white matter (NAWM). During the course of the disease, the proportion of smouldering lesions increases over time and is higher in progressive than in relapsing–remitting disease. These lesions have also been shown to correlate with disability and predict progression in both relapsing–remitting and secondary progressive SM. It is important to revise the current disease classification system, clinical trial designs, and trial endpoints. Furthermore, novel molecular biomarkers (like NfL, GFAP, CHI3L, CXCL13, kynurenines, redox molecules, etc.) help the decision about the optimal treatment of MS patients.

Prof. Dr. László Vécsei
Guest Editor

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Keywords

  • progression-independent relapses (PIRAs)
  • smouldering-associated worsening (SAW)
  • lack of new relapses and of new magnetic resonance imaging activity (NEIDA)
  • slowly expanding lesions (SEL)
  • no evidence of smouldering disease activity (NESDA)
  • neurofilament (NfL)
  • glial fibrillary acidic protein (GFAP)
  • patient-reported outcome (PRO)
  • paramagnetic rim lesions (PRLs)
  • relapse-associated worsening (RAW)

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