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Pathophysiological Insights, Biomarkers and New Therapeutic Strategies in Immune-Mediated Disorders and Neurodegenerative Diseases

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

Deadline for manuscript submissions: 20 September 2026 | Viewed by 4873

Special Issue Editor

Dr. Eleonora Virgilio

E-Mail Website
Guest Editor
Neurology Unit, Department of Clinical and Biological Sciences, University Hospital San Luigi Gonzaga, University of Turin, 10043 Turin, Italy
Interests: multiple sclerosis; cognition; biomarkers; neuroimmunology

Special Issue Information

Dear Colleagues,

Neurodegenerative disorders are progressive and disabling diseases resulting in motor and cognitive disability, secondary to progressive neuronal loss with a high impact on quality of life. Moreover,  immune system dysregulation and inflammatory patterns have been recognized as involved in several neurodegenerative diseases, not only autoimmune and demyelinating ones. Although inflammation may not represent the only pathological mechanism of neurodegenerative processes, it could play a crucial effect on disease progression. Further improvement research is needed to unravel and clarify new pathophysiological mechanisms and therapeutic strategies for neurodegenerative and immune-mediated neurological disorders. Also, reliable diagnostic, prognostic, and predictive biomarkers would be essential to advancing precision medicine.

This Special Issue aims to highlight current knowledge regarding pathophysiological mechanisms, fluid biomarkers, and new therapeutic strategies in neurological diseases. Authors are welcome to cover all areas of clinical neurology, including neurodegenerative diseases and immune-mediated disorders of central and peripheral nervous system. Both original articles and reviews are welcome.

I look forward to receiving your contributions.

Dr. Eleonora Virgilio
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • neurodegeneration
  • neuroimmunology
  • inflammation
  • biomarkers
  • treatment
  • pathophysiology
  • multiple sclerosis
  • myasthenia gravis
  • neurodegenerative disease

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Published Papers (2 papers)

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Review

22 pages, 2955 KB  
Review
C-Reactive Protein and Neurological Autoimmune Diseases: Bridging the Diagnostic and Pathogenic Gap
by Patrik Buzgau, Mark Slevin, Ioana Theodora Barna, Lóránd Dénes, Amelia Tero-Vescan, Aurelio Pio Russo and Ylenia Pastorello
Int. J. Mol. Sci. 2026, 27(3), 1322; https://doi.org/10.3390/ijms27031322 - 28 Jan 2026
Viewed by 1183
Abstract
C-reactive protein (CRP) has emerged as a crucial link between systemic and neuroinflammatory processes, though its role across neurological autoimmune disorders remains incompletely understood. Pathologies such as multiple sclerosis (MS), neuromyelitis optica spectrum disorder (NMOSD), Guillain–Barré syndrome (GBS), and myasthenia gravis (MG) share [...] Read more.
C-reactive protein (CRP) has emerged as a crucial link between systemic and neuroinflammatory processes, though its role across neurological autoimmune disorders remains incompletely understood. Pathologies such as multiple sclerosis (MS), neuromyelitis optica spectrum disorder (NMOSD), Guillain–Barré syndrome (GBS), and myasthenia gravis (MG) share chronic, dysregulated inflammation resulting from loss of immune tolerance. Their pathogenesis arises from interactions among genetic susceptibility, environmental factors, and gut microbiota alterations that trigger autoreactive immune cascades through molecular mimicry, ectopic antigen expression, or paraneoplastic cross-reactivity. These immune pathways sustain inflammation and promote neuroaxonal injury. CRP, synthesized mainly by hepatocytes in response to interleukin-6 (IL-6), functions as both an effector and reporter of inflammation, linking systemic immune activation to neuroinflammatory damage. Elevated CRP levels correlate with unfavorable outcomes, including accelerated disability in MS, IL-6-mediated astrocyte injury in NMOSD, respiratory failure in GBS, and crisis susceptibility in MG. Composite indices such as the CRP-to-albumin ratio are emerging as refined prognostic markers, though interpretation is limited by non-specificity and biological variability. This review integrates current evidence on CRP’s mechanistic roles, clinical associations, and translational potential in neuroinflammatory disorders, combining molecular, clinical, and imaging perspectives to refine its role within inflammation-driven neurodegeneration. Full article
(This article belongs to the Special Issue Pathophysiological Insights, Biomarkers and New Therapeutic Strategies in Immune-Mediated Disorders and Neurodegenerative Diseases)
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16 pages, 487 KB  
Review
TNFR2 Agonism: Basic Science and Promising Treatment for Multiple Sclerosis and Related Diseases
by Denise L. Faustman, Miriam Davis and Willem M. Kuhtreiber
Int. J. Mol. Sci. 2025, 26(16), 7839; https://doi.org/10.3390/ijms26167839 - 14 Aug 2025
Cited by 3 | Viewed by 2914
Abstract
The three pathological hallmarks of multiple sclerosis (MS) are inflammation, demyelination, and progressive neurodegeneration. None of the approved disease-modifying therapies for MS counters all three pathologies, and, more specifically, none is approved for neuroprotection. Axonal loss is the most significant contributor to chronic [...] Read more.
The three pathological hallmarks of multiple sclerosis (MS) are inflammation, demyelination, and progressive neurodegeneration. None of the approved disease-modifying therapies for MS counters all three pathologies, and, more specifically, none is approved for neuroprotection. Axonal loss is the most significant contributor to chronic and irreversible disability in MS. A tantalizing molecular target has emerged to uniquely counter all three MS pathologies: tumor necrosis factor receptor 2 (TNFR2). Agonism or activation of TNFR2 has been shown in MS models to induce immunosuppression, oligodendrocyte precursor differentiation, and neuroprotection. Further, in basic science studies stemming from the past 15 years, TNFR2 agonism is known to be a strong inducer of T-regulatory cells (Tregs). Treg cells, and especially those expressing TNFR2, are known to confer the strongest suppression per cell type. TNFR2 is even more attractive as a therapeutic target because of its restricted expression by only a handful of CNS and immune cell subsets, thereby minimizing the likelihood of systemic and other adverse effects. Recent antibody design work suggests many of the hurdles of Treg agonism may have been overcome. This review covers the current treatment landscape for MS, the basic science of TNFR2, the rationale for and evidence behind TNFR2 agonism to treat multiple sclerosis, the design of potent TNFR2 agonist antibodies, and the treatment applications for other neurological, autoimmune, or inflammatory diseases. Full article
(This article belongs to the Special Issue Pathophysiological Insights, Biomarkers and New Therapeutic Strategies in Immune-Mediated Disorders and Neurodegenerative Diseases)
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