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Molecular Mechanisms and Translational Insights in Neurological Disorders
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Molecular Mechanisms and Translational Insights in Neurological Disorders

A Special Issue of International Journal of Molecular Sciences (ISSN 1422-0067) belonging to the section "Molecular Neurobiology".

Deadline for manuscript submissions: 31 December 2026 | Viewed by 6346

Editor

Dr. Tiago Santos

E-Mail Website
Guest Editor
School of Medicine, University of Minho, 4710-057 Braga, Portugal
Interests: neuroprotection; neural stem cells; neurodegenerative diseases; neurodevelopmental disorders; neurogenesis; central nervous system; neuroblasts
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue focuses on the molecular mechanisms that drive neurological disorders and their translation into novel therapies. We welcome contributions that elucidate how molecular insights can accelerate the design of more effective and targeted treatments. The scope covers major neurological conditions such as neurodegenerative diseases (e.g., Alzheimer’s and Parkinson’s); neuroinflammatory, demyelinating, and cerebrovascular conditions; neurodevelopmental disorders; mood and anxiety disorders; and spinal cord and traumatic brain injuries. Submissions may explore genetic, epigenetic, transcriptomic, proteomic, metabolomic, or immunomolecular aspects; identify and validate biomarkers; reveal novel therapeutic targets; or evaluate delivery platforms that bridge basic molecular research and clinical application. Studies employing patient-derived models, organoids, high-throughput screening, systems biology, or computational approaches integrated with molecular data are also encouraged. By gathering such interdisciplinary work, this Special Issue aims to provide a state-of-the-art overview of how molecular discoveries can accelerate precision neurology and improve patient outcomes.

Dr. Tiago Santos
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-anonymized 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

  • neurological disorders
  • molecular mechanisms
  • translational neuroscience
  • drug targets
  • biomarkers
  • neurodegenerative disorders
  • neuroinflammatory conditions
  • demyelinating conditions
  • cerebrovascular conditions
  • neurodevelopmental disorders
  • mood disorders
  • anxiety disorders
  • spinal cord injury
  • traumatic brain injury
  • precision neurology
  • therapeutic development

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Published Papers (5 papers)

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Review

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34 pages, 2178 KB  
Review
Transcriptomics Insights into Spinal Cord Injury for Therapy Development
by Daria Chudakova, Olga Astakhova, Matthew Shkap, Ekaterina Levichkina, Alesya Soboleva, Artur Biktimirov and Vladimir Baklaushev
Int. J. Mol. Sci. 2026, 27(13), 5870; https://doi.org/10.3390/ijms27135870 - 29 Jun 2026
Viewed by 778
Abstract
Traumatic spinal cord injury (SCI) is a severe medical condition, often resulting in permanent disability, with significant impacts on patients’ quality of life and burden on healthcare systems. Current therapeutic approaches for SCI are insufficient, advocating for the development of more effective treatments. [...] Read more.
Traumatic spinal cord injury (SCI) is a severe medical condition, often resulting in permanent disability, with significant impacts on patients’ quality of life and burden on healthcare systems. Current therapeutic approaches for SCI are insufficient, advocating for the development of more effective treatments. As changes in transcriptome post-SCI can provide clues for novel treatment strategies and targets, substantial efforts have been made recently to characterize such transcriptional changes and their spatiotemporal features. This narrative review focuses on how transcriptomics, alone or in combination with other omics data, can contribute to understanding SCI pathobiology and the mechanisms of post-SCI regeneration and guide the development of novel SCI therapies. It covers an arsenal of tools for transcriptomics studies and provides a concise summary of findings from the latest relevant studies (predominantly from 2020 to 2025), representing the major directions in the field. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Translational Insights in Neurological Disorders)
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37 pages, 2940 KB  
Review
Trends in the Engineering of Adeno-Associated Virus (AAV) for Precision Gene Delivery to the Central Nervous System (CNS)
by Sola Oloruntimehin and Alexander Malogolovkin
Int. J. Mol. Sci. 2026, 27(13), 5668; https://doi.org/10.3390/ijms27135668 - 23 Jun 2026
Viewed by 1266
Abstract
Rare genetic disorders of the central nervous system (CNS) remain some of the most complex and challenging diseases to treat for several reasons. Targeting the CNS, especially the brain, presents one of the greatest obstacles in gene therapy using adeno-associated virus (AAV) vectors. [...] Read more.
Rare genetic disorders of the central nervous system (CNS) remain some of the most complex and challenging diseases to treat for several reasons. Targeting the CNS, especially the brain, presents one of the greatest obstacles in gene therapy using adeno-associated virus (AAV) vectors. Although various AAVs have been identified for their ability to transduce different cells in the CNS, their effectiveness and efficiency are significantly limited by the presence of neutralising antibodies (NAbs) and restricted cargo capacity. Despite these challenges, our understanding of AAV structure and technological advances continue to enable researchers to develop innovative strategies that have resulted in groundbreaking, FDA-approved therapeutic products now available for Leber congenital amaurosis (LCA) (Luxturna®), spinal muscular atrophy (SMA) (Zolgensma®), and the two recent gene therapy products for aromatic L-amino acid decarboxylase (AADC) deficiency, Kebilidi® and Upstaza®, which currently hold FDA and EMA approval, respectively. This review aims to highlight recent advances in the field of AAV gene therapy for neurological disorders, identify research gaps, and suggest areas for future investigation to enable potential breakthroughs particularly in neurodegenerative, neurodevelopmental, and neuromuscular disorders. We foresee that more tissue- and cell-specific AAV vectors designed using AI-powered platforms will emerge to precisely and efficiently target specific brain regions, transforming how CNS disorders are treated. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Translational Insights in Neurological Disorders)
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36 pages, 11488 KB  
Review
Lipid Metabolism Reprogramming in the Aging Brain: Glial-Mediated Pathogenic Mechanisms and Translational Strategies in Neurodegeneration
by Wei Shao, Kai Wang, Yongchao Liu, Haojia Zhang, Zijin Sun and Rui Zhou
Int. J. Mol. Sci. 2026, 27(12), 5580; https://doi.org/10.3390/ijms27125580 - 20 Jun 2026
Viewed by 1216
Abstract
The mammalian brain fundamentally relies on precise lipid homeostasis to maintain structural integrity and complex neural signaling. Emerging evidence positions lipid metabolism reprogramming not merely as a secondary pathological byproduct but as a core initiating driver of age-related neurodegenerative diseases. This review systematically [...] Read more.
The mammalian brain fundamentally relies on precise lipid homeostasis to maintain structural integrity and complex neural signaling. Emerging evidence positions lipid metabolism reprogramming not merely as a secondary pathological byproduct but as a core initiating driver of age-related neurodegenerative diseases. This review systematically evaluates the mechanisms of cerebral lipid dyshomeostasis during brain aging, highlighting glial cells as the central mediators of this pathological cascade. We comprehensively dissect the age-associated “lipid drift”, emphasizing apolipoprotein E (APOE)-induced cholesterol transport defects and lipid raft pathology, the accumulation of lipid droplets that triggers microglial metabolic stress (LDAMs), and ceramide-driven neuronal apoptosis coupled with the exosome-mediated propagation of pathogenic proteins. Furthermore, we map these aberrant lipid networks to specific pathological signatures in Alzheimer’s, Parkinson’s, and demyelinating diseases. Finally, we critically evaluate promising therapeutic interventions, including nutritional strategies, LXR/RXR agonists, and nanotechnology-enabled delivery systems designed to bypass the blood–brain barrier. By integrating high-throughput lipidomics for early diagnostic biomarker discovery, we underscore the translational imperative of restoring cerebral lipid homeostasis as a disease-modifying strategy for neurodegeneration. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Translational Insights in Neurological Disorders)
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15 pages, 490 KB  
Review
Repurposing Antidiabetic Medications for Parkinson’s Disease: Focus on Biomarker Strategies for Disease Modification
by Narayana K. Yelleswarapu and Christos Sidiropoulos
Int. J. Mol. Sci. 2026, 27(6), 2560; https://doi.org/10.3390/ijms27062560 - 11 Mar 2026
Cited by 1 | Viewed by 1458
Abstract
Parkinson’s disease (PD) is a progressive neurodegenerative disorder. It shares many pathophysiologic similarities with type 2 diabetes mellitus (T2DM). Numerous studies have explored the repurposing of antidiabetic medications for their potential neuroprotective effects in PD. There has not been a consolidated review of [...] Read more.
Parkinson’s disease (PD) is a progressive neurodegenerative disorder. It shares many pathophysiologic similarities with type 2 diabetes mellitus (T2DM). Numerous studies have explored the repurposing of antidiabetic medications for their potential neuroprotective effects in PD. There has not been a consolidated review of the biochemical biomarkers that have been evaluated across antidiabetic medications. This review aims to assess the current landscape of biomarker research in evaluating the efficacy of these antidiabetic agents as disease-modifying therapies in PD. We examine the molecular mechanisms targeted by these drugs, the biomarkers used to assess their effects, and the outcomes of clinical trials. This review hopes to identify gaps in current research and enhance the evaluation of antidiabetic medications in PD. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Translational Insights in Neurological Disorders)
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Other

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17 pages, 1842 KB  
Case Report
B-Cell Depletion as Evidence for Shared Neuroimmune Pathways in Combined Central and Peripheral Demyelination: A Case Report and Literature Review
by Laura-Elena Cucu, Alina Săcărescu, Cristina Grosu, Victor Constantinescu, Laura Cristina Baciu, Gabriela-Smărăndița Asaftei-Titianu, Cristina Gațcan, Costin Chirica, Otilia Elena Frăsinariu and Emilian Bogdan Ignat
Int. J. Mol. Sci. 2026, 27(6), 2810; https://doi.org/10.3390/ijms27062810 - 20 Mar 2026
Viewed by 946
Abstract
Combined central and peripheral demyelination (CCPD) is a rare neuroimmunological condition involving inflammatory demyelination of both the central nervous system (CNS) and peripheral nervous system (PNS). We report a chronic progressive CCPD case initially diagnosed as chronic inflammatory demyelinating polyneuropathy (CIDP) and treated [...] Read more.
Combined central and peripheral demyelination (CCPD) is a rare neuroimmunological condition involving inflammatory demyelination of both the central nervous system (CNS) and peripheral nervous system (PNS). We report a chronic progressive CCPD case initially diagnosed as chronic inflammatory demyelinating polyneuropathy (CIDP) and treated with conventional CIDP-directed immunotherapies, with subsequent development of multiple sclerosis (MS)-like CNS demyelination. An extensive diagnostic evaluation excluded alternative infectious, metabolic, paraneoplastic, and antibody-mediated etiologies affecting either compartment. In the absence of a unifying pathogenic autoantibody, the combined clinical, radiological, cerebrospinal fluid, and electrophysiological findings support a shared immune-mediated process. Within this framework, B cells are implicated through antibody-independent mechanisms, including antigen presentation, pro-inflammatory cytokine production (e.g., IL-6), and amplification of Th1/Th17-driven inflammation. Interactions between B cells and the complement system via CR1 (CD35) and CR2 (CD21), together with dysfunction of the blood–brain barrier (BBB) and blood–nerve barrier (BNB), may facilitate parallel immune activation across both compartments. In this case, the observed radiological and electrophysiological stabilization under anti-CD20 therapy is consistent with a B-cell-driven pathogenic model in CCPD. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Translational Insights in Neurological Disorders)
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