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Neurology International
Special Issues
Molecular Research of CNS Diseases and Neurological Disorders
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Molecular Research of CNS Diseases and Neurological Disorders

A special issue of Neurology International (ISSN 2035-8377). This special issue belongs to the section "Movement Disorders and Neurodegenerative Diseases".

Deadline for manuscript submissions: 28 February 2026 | Viewed by 3993

Special Issue Editor

Dr. Chakrapani Vemulawada

E-Mail Website
Guest Editor
Department of Pathology, The University of Iowa, Iowa City, IA, USA
Interests: immunology; T cell biology; molecular biology; neuroimmunology; genome editing

Special Issue Information

Dear Colleagues,

This Special Issue aims to highlight cutting-edge advancements and insights into the molecular mechanisms underlying central nervous system (CNS) diseases and neurological disorders, fostering a deeper understanding that could pave the way for novel diagnostics and therapeutics.

Scope and Topics:

We invite original research articles, reviews, and short communications addressing, but not limited to, the following:

  • Molecular pathways involved in neurodegenerative diseases such as Alzheimer’s, Parkinson’s, and Huntington’s disease and autoimmune immune diseases such as Multiple Sclerosis, T1D, and RA.
  • Advances in molecular imaging and biomarker identification.
  • Mechanisms of neuroinflammation and its role in CNS disorders.
  • Genetic and epigenetic regulation in neurological conditions.
  • Molecular targets for novel pharmacological interventions.
  • Insights into CNS injury, repair, and neuroplasticity.
  • Translational research bridging molecular findings with clinical applications.

Authors are encouraged to submit high-quality manuscripts that contribute significantly to the field. Article types include original articles, reviews, case reports, communications, etc.

Dr. Chakrapani Vemulawada
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. Neurology International is an international peer-reviewed open access monthly 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 1800 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

  • autoimmunity
  • CNS disorders
  • neurodegenerative diseases
  • immunopathology
  • brain injury
  • T cell biology
  • immune dysregulation
  • molecular biology

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  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • Reprint: MDPI Books provides the opportunity to republish successful Special Issues in book format, both online and in print.

Further information on MDPI's Special Issue policies can be found here.

Published Papers (2 papers)

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Research

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15 pages, 1648 KB  
Article
The Concomitant Effect of the Antiepileptic Drug Lacosamide and rTMS on an SH-SY5Y Model of Neuronal Excitability
by Ioannis Dardalas, Efstratios K. Kosmidis, Vasilios K. Kimiskidis, Roza Lagoudaki, Theodoros Samaras, Theodoros Moysiadis, Dimitrios Kouvelas and Chryssa Pourzitaki
Neurol. Int. 2025, 17(10), 152; https://doi.org/10.3390/neurolint17100152 - 24 Sep 2025
Viewed by 814
Abstract
Background/Objectives: Epilepsy is identified by irregular neuronal hyperexcitability, generating recurrent seizures. Despite many available pharmacological treatments, certain patients with drug-resistant epilepsy may require novel therapeutic approaches. In the present study, we aimed to evaluate the effects of lacosamide, low-frequency repetitive transcranial magnetic [...] Read more.
Background/Objectives: Epilepsy is identified by irregular neuronal hyperexcitability, generating recurrent seizures. Despite many available pharmacological treatments, certain patients with drug-resistant epilepsy may require novel therapeutic approaches. In the present study, we aimed to evaluate the effects of lacosamide, low-frequency repetitive transcranial magnetic stimulation, and their combination on intracellular calcium dynamics in an in vitro model of neuronal excitability, hypothesizing that these interventions could mitigate potassium chloride-induced neuronal excitation. Methods: We utilized differentiated SH-SY5Y human neuroblastoma cells as an in vitro model of neuronal excitability. Neuronal excitability was induced with 50 mM KCl, and cells were treated with lacosamide (300 µM), rTMS (1 Hz), or their combination. Intracellular calcium levels were quantified using fluo-4 AM fluorescence calcium imaging, with changes expressed as percentage change in fluorescence intensity (%ΔF/F) relative to baseline. Results: The combination of lacosamide and rTMS was the most effective, significantly reducing KCl-induced calcium elevation (ΔF/F = 9.15) compared to lacosamide alone (ΔF/F = 17.11), rTMS alone (ΔF/F = 23.70), and the untreated cells serving as controls (ΔF/F = 66.70). The combination showed a statistically significant effect, with enhanced suppression of neuronal excitability compared to individual treatments. Conclusions: Lacosamide and low-frequency rTMS (1 Hz) effectively attenuated KCl-induced changes in intracellular calcium levels in vitro, with their combination demonstrating the highest efficacy. These findings suggest a promising foundation in the management of drug-resistant epilepsy. Future studies are necessitated to validate these results and benefit clinical translation. Full article
(This article belongs to the Special Issue Molecular Research of CNS Diseases and Neurological Disorders)
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Review

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41 pages, 614 KB  
Review
Glial Cells in Spinal Muscular Atrophy: Speculations on Non-Cell-Autonomous Mechanisms and Therapeutic Implications
by Andrej Belančić, Tamara Janković, Elvira Meni Maria Gkrinia, Iva Kristić, Jelena Rajič Bumber, Valentino Rački, Kristina Pilipović, Dinko Vitezić and Jasenka Mršić-Pelčić
Neurol. Int. 2025, 17(3), 41; https://doi.org/10.3390/neurolint17030041 - 13 Mar 2025
Cited by 4 | Viewed by 2797
Abstract
Spinal muscular atrophy (SMA) is a neuromuscular disorder caused by homozygous deletions or mutations in the SMN1 gene, leading to progressive motor neuron degeneration. While SMA has been classically viewed as a motor neuron-autonomous disease, increasing evidence indicates a significant role of glial [...] Read more.
Spinal muscular atrophy (SMA) is a neuromuscular disorder caused by homozygous deletions or mutations in the SMN1 gene, leading to progressive motor neuron degeneration. While SMA has been classically viewed as a motor neuron-autonomous disease, increasing evidence indicates a significant role of glial cells—astrocytes, microglia, oligodendrocytes, and Schwann cells—in the disease pathophysiology. Astrocytic dysfunction contributes to motor neuron vulnerability through impaired calcium homeostasis, disrupted synaptic integrity, and neurotrophic factor deficits. Microglia, through reactive gliosis and complement-mediated synaptic stripping, exacerbate neurodegeneration and neuroinflammation. Oligodendrocytes exhibit impaired differentiation and metabolic support, while Schwann cells display abnormalities in myelination, extracellular matrix composition, and neuromuscular junction maintenance, further compromising motor function. Dysregulation of pathways such as NF-κB, Notch, and JAK/STAT, alongside the upregulation of complement proteins and microRNAs, reinforces the non-cell-autonomous nature of SMA. Despite the advances in SMN-restorative therapies, they do not fully mitigate glial dysfunction. Targeting glial pathology, including modulation of reactive astrogliosis, microglial polarization, and myelination deficits, represents a critical avenue for therapeutic intervention. This review comprehensively examines the multifaceted roles of glial cells in SMA and highlights emerging glia-targeted strategies to enhance treatment efficacy and improve patient outcomes. Full article
(This article belongs to the Special Issue Molecular Research of CNS Diseases and Neurological Disorders)
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