Molecular Research of CNS Diseases and Neurological Disorders

A special issue of Neurology International (ISSN 2035-8377).

Deadline for manuscript submissions: 31 July 2025 | Viewed by 487

Special Issue Editor


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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 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. 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 1600 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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Published Papers (1 paper)

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Review

41 pages, 614 KiB  
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
Viewed by 334
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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