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Molecular Mechanisms and Translational Insights in Neurological Disorders

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

Deadline for manuscript submissions: 31 December 2026 | Viewed by 1359

Special Issue Editor


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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
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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

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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 (2 papers)

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Review

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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
Viewed by 514
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
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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 466
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
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