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Clinical Advances in Multiple Sclerosis 2.0
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Clinical Advances in Multiple Sclerosis 2.0

A special issue of Journal of Clinical Medicine (ISSN 2077-0383). This special issue belongs to the section "Clinical Neurology".

Deadline for manuscript submissions: closed (15 April 2024) | Viewed by 2648

Special Issue Editor

Prof. Dr. Konrad Rejdak

E-Mail Website
Guest Editor
President of Polish Neurological Society, Department of Neurology, Medical University of Lublin, 20‐954 Lublin, Poland
Interests: clinical neurology; demyelinating diseases; neuroinflammation; biomarkers
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Multiple sclerosis is an inflammatory, autoimmune-mediated chronic disease that affects the central nervous system in young adults. Despite extensive research, its exact etiology remains unknown, but there has been great progress in understanding its pathogenesis. Similarly, cutting edge technology has been introduced for the discovery of novel diagnostic tools and new drugs targeting different aspects of complex pathogenic mechanisms. There are several major unmet needs in the understanding and management of MS: the neurodegenerative component of MS pathogenesis remains an enigma, novel specific and sensitive biomarkers and imaging techniques to monitor disease activity and progression are needed, and new drugs with high efficacy and a good safety profile are required to stop the neurodegenerative process as well as provide regenerative potential.

Given the enormous success of the First Edition (https://www.mdpi.com/journal/jcm/special_issues/Clinical_Advances_Multiple_Sclerosis), I believe that it is time to move forward to the Second Edition of this Special Issue. This Second Edition will focus on recent advances in the pathogenesis, diagnostic/disease monitoring methods, and treatment of MS. We plan to include reviews (updates on the pathogenesis of MS, prodromal multiple sclerosis, biomarkers, high field MRI imaging, novel drugs in the pipeline) and original papers detailing novel biomarkers and clinical research.

Prof. Dr. Konrad Rejdak
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 100 words) can be sent to the Editorial Office for announcement on this website.

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. Journal of Clinical Medicine is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). 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

  • multiple sclerosis
  • biomarkers
  • high field MRI techniques
  • novel drugs in the pipeline
  • diagnosis and treatment

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Related Special Issue

Published Papers (2 papers)

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Research

13 pages, 264 KiB  
Article
TNF-alfa Gene Polymorphism Associations with Multiple Sclerosis
by Lukas Kalvaitis, Greta Gedvilaite-Vaicechauskiene, Loresa Kriauciuniene, Renata Balnyte and Rasa Liutkeviciene
J. Clin. Med. 2024, 13(13), 3693; https://doi.org/10.3390/jcm13133693 - 25 Jun 2024
Viewed by 964
Abstract
Background: TNF-α has a dual role in multiple sclerosis (MS), contributing to both protective and harmful effects. It activates immune cells, promotes the formation of inflammatory lesions in the central nervous system, and stimulates the production of other pro-inflammatory cytokines and chemokines, [...] Read more.
Background: TNF-α has a dual role in multiple sclerosis (MS), contributing to both protective and harmful effects. It activates immune cells, promotes the formation of inflammatory lesions in the central nervous system, and stimulates the production of other pro-inflammatory cytokines and chemokines, leading to myelin destruction and neuronal damage. Our research focused on investigating the relationship between TNF-alpha (rs1800630, rs1800629, and rs361525) gene polymorphisms and MS. Methods: 250 healthy controls and 250 multiple sclerosis (MS) patients were included in the study. DNA was extracted from leucocytes from peripheral venous blood by salt precipitation. Single nucleotide polymorphisms (SNPs) were tested using RT–PCR. Statistical analysis of the data was performed using IBM SPSS Statistics 29.0 data analysis software. Results: The analysis revealed that the rs361525 AG genotype was significantly less frequent in the MS group compared to the control group (4.0% vs. 7.2%, p = 0.042). Sex-specific analysis showed a significant difference in genotype distribution (GG, AG, AA) among males between the MS group and the control group (97.7%, 0%, 2.3% vs. 90.6%, 9.4%, 0%, p = 0.005). For the rs1800629 polymorphism, significant results were also found. In subjects younger than 39 years, the A allele was significantly less frequent in the MS group than in the control group (8.6% vs. 15.0%, p = 0.030). The most robust model indicated that the AA genotype reduced the odds of MS by approximately 2 fold compared to the AG + GG genotype (p = 0.044), and each A allele reduced the odds of MS by approximately 2 fold (p = 0.028). The rs1800630 A allele was significantly more common in males in the MS group than in the control group (21.0% vs. 12.9%, p = 0.046). Conclusions: In conclusion, our study identifies significant associations between TNF-alpha gene variants and MS. Specifically, the rs631525 AG genotype was less common in the MS group, with notable sex-specific differences observed. The rs1800629 A allele was statistically significantly less frequent in the MS group than in the control group, and the AA genotype reduced the odds of MS occurrence by ~2 fold compared with the AG + GG genotypes. Additionally, each A allele of rs1800629 was linked to a 2-fold decreased odds of MS occurrence. In males, the rs1800630 A allele was more frequent in the MS group. These findings highlight the relevance of TNF-alpha genetic variations in MS susceptibility, suggesting potential avenues for further research and therapeutic exploration. Full article
(This article belongs to the Special Issue Clinical Advances in Multiple Sclerosis 2.0)
11 pages, 1590 KiB  
Article
Exploring the Potential of the Corpus Callosum Area as a Predictive Marker for Impaired Information Processing in Multiple Sclerosis
by Shun Akaike, Tomoko Okamoto, Ryoji Kurosawa, Nozomi Onodera, Youwei Lin, Wakiro Sato, Takashi Yamamura and Yuji Takahashi
J. Clin. Med. 2023, 12(21), 6948; https://doi.org/10.3390/jcm12216948 - 6 Nov 2023
Viewed by 1268
Abstract
Early cognitive impairment (CI) detection is crucial in multiple sclerosis (MS). However, it can progress silently regardless of relapse activity and reach an advanced stage. We aimed to determine whether the corpus callosum area (CCA) is a sensitive and feasible marker for CI [...] Read more.
Early cognitive impairment (CI) detection is crucial in multiple sclerosis (MS). However, it can progress silently regardless of relapse activity and reach an advanced stage. We aimed to determine whether the corpus callosum area (CCA) is a sensitive and feasible marker for CI in MS compared to other neuroimaging markers. We assessed cognitive function in 77 MS patients using the Symbol Digit Modalities Test, Paced Auditory Serial Additions Task, Wechsler Adult Intelligence Scale-IV, and Wechsler Memory Scale-Revised. The neuroimaging markers included manually measured CCA, two diffusion tensor imaging markers, and nine volumetric measurements. Apart from volumes of the hippocampus and cerebellum, ten markers showed a significant correlation with all neuropsychological tests and significant differences between the groups. The normalized CCA demonstrated a moderate-to-strong correlation with all neuropsychological tests and successfully differentiated between the CI and cognitively normal groups with 80% sensitivity and 83% specificity. The marker had a large area under the curve and a high Youden index (0.82 and 0.63, respectively) and comparability with established cognitive markers. Therefore, the normalized CCA may serve as a reliable marker for CI in MS and can be easily implemented in clinical practice, providing a supportive diagnostic tool for CI in MS. Full article
(This article belongs to the Special Issue Clinical Advances in Multiple Sclerosis 2.0)
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