Multiple Sclerosis: Diagnosis and Treatment—3rd Edition

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Neurobiology and Clinical Neuroscience".

Deadline for manuscript submissions: 31 August 2025 | Viewed by 397

Special Issue Editor


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Guest Editor
Department of Neurology, Baylor College of Medicine, Houston, TX 77030, USA
Interests: demyelinating disorders; multiple sclerosis; epidemiology and genetic aspects; therapeutic trials
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Special Issue Information

Dear Colleagues,

This Special Issue is the third volume of our previous Special Issue “Multiple Sclerosis: Diagnosis and Treatment”. Multiple Sclerosis (MS), an inflammatory demyelinating disease of the CNS, has acquired world-wide recognition with its increasing global prevalence, including populations previously considered not to be commonly affected. Genetics and environmental factors play a determining role in its pathogenesis. Notable progress has been accomplished in diagnostic criteria (which evolve continuously) as well as therapeutic advances. In fact, in less than three decades, more therapies with diverse mechanisms of action (MOAs) for relapsing and progressive MS have been developed for MS than for any other neurological disorder. Magnetic resonance imaging (MRI), the golden tool for diagnosis, is essential for monitoring the evolution of the disease and the response to therapy. Advanced MR techniques are being investigated in MS to be translated into clinical applications and machine learning to improve diagnostic sensitivity. Other aspects requiring special attention are the role of intestinal microbiota and the immunologic mechanisms present in MS.   

Despite this progress, substantial challenges have arisen, including the need for differential diagnosis with respect to other major inflammatory/demyelinating disorders that have been identified relatively recently (totally different in mechanism and management), such as neuromyelitis optica spectrum disorder (NMOSD) and anti-MOG syndromes, and the role of environment and epigenetic factors in the mechanism of MS. A common clinical manifestation affecting all forms of the disease is the presence of cognitive dysfunction requiring special attention, identification and management. This constitutes the most common cause of employment disability affecting young individuals with MS.  

We cordially invite authors and investigators within this complex field of universal interest to submit original research or review articles pertaining to this Special Issue. Studies and opinions on risk factors related to the development of the disease, molecular aspects of its pathogenesis, diagnostic intricacies despite current criteria, and the status of disease-modifying therapies’ effects in the Radiologically Isolated Syndrome (RIS), prodromic, relapsing and progressive forms of MS, and what is foreseen on the horizon are welcome, including management of pediatric demyelinating disease and in the aging individual.

Prof. Dr. Víctor M. Rivera
Guest Editor

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Keywords

  • multiple sclerosis
  • pathogenesis
  • progressive MS
  • MRI
  • disease-modifying therapies
  • demyelinating disorders
  • cognitive dysfunction
  • intestinal microbiota

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14 pages, 14167 KiB  
Article
Laser-Induced Cortical Lesions in Mice as a Model for Progressive Multiple Sclerosis Pathology
by Bhavya Ojha, Bita Ramazani, Rouhin Belal, Jonathan Krieger, Maria Bloksgaard, Gabriela Teresa Lyszczarz, Dominika Rusin, Agnieszka Wlodarczyk, Una FitzGerald, Trevor Owens and Reza Khorooshi
Biomedicines 2025, 13(5), 1195; https://doi.org/10.3390/biomedicines13051195 - 14 May 2025
Viewed by 289
Abstract
Background: The current animal models of multiple sclerosis (MS) predominantly emphasize white matter inflammation, reflecting early-stage disease. However, progressive MS (PMS) is characterized by cortical pathology, including subpial demyelination, chronic meningeal inflammation, and microglial activation, which are underrepresented in the existing models. While [...] Read more.
Background: The current animal models of multiple sclerosis (MS) predominantly emphasize white matter inflammation, reflecting early-stage disease. However, progressive MS (PMS) is characterized by cortical pathology, including subpial demyelination, chronic meningeal inflammation, and microglial activation, which are underrepresented in the existing models. While alternative mouse models replicate the relapsing–remitting phenotype and gray matter pathology, pathology is frequently dispersed throughout the brain, complicating the analysis of the specific lesion sites. Methods: To address this gap, we developed a novel model that integrates laser-induced focal demyelination with cytokine-driven meningeal inflammation to replicate the key aspects of PMS cortical pathology. Results: Using two-photon laser irradiation, we induced controlled subpial cortical lesions in CX3CR1-GFP mice, leading to microglial activation, astrocytosis, and focal demyelination. The addition of IFNγ-expressing adenovirus to promote meningeal inflammation which resulted in prolonged glial responses, increased immune cell infiltration, and exacerbated demyelination, mimicking the PMS-associated pathology. Conclusions: This model provides a powerful tool to investigate the mechanisms underlying the cortical lesion development and immune-mediated neurodegeneration in PMS. By capturing the critical aspects of cortical pathology, it enables the evaluation of therapeutic strategies targeting neuroinflammation and demyelination, ultimately aiding in the development of new treatments of progression in PMS patients. Full article
(This article belongs to the Special Issue Multiple Sclerosis: Diagnosis and Treatment—3rd Edition)
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