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Advances in the Fields of Neurotrauma and Neuroregeneration
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Advances in the Fields of Neurotrauma and Neuroregeneration

A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Neuroscience".

Deadline for manuscript submissions: 31 October 2025 | Viewed by 24452

Special Issue Editors

Dr. Alexander Younsi

E-Mail Website
Guest Editor
Department of Neurosurgery, Heidelberg University Hospital, INF 400, 69120 Heidelberg, Germany
Interests: neurotrauma; spinal cord injury; traumatic brain injury; neuroregeneration; neuroprotection
Dr. Guoli Zheng

E-Mail Website
Guest Editor
Department of Neurosurgery, University Hospital Heidelberg, University of Heidelberg, INF 400, 69120 Heidelberg, Germany
Interests: neurotrauma; spinal cord injury; traumatic brain injury; neuroregeneration; neurobehavioral analysis
Dr. Xing Cheng

E-Mail Website
Guest Editor
1. Guangdong Provincial Key Laboratory of Orthopaedics and Traumatology, Guangzhou, China
2. The 1st. Affiliated Hospital of Sun Yat-Sen University, Guangzhou, China
Interests: spinal cord injury; neuropathic pain; neuroregeneration; neural rehabilitation; behavioral analysis

Special Issue Information

Dear Colleagues, 

Neurotrauma, which mostly refers to traumatic brain injury (TBI) or spinal cord injury (SCI), is a world-wide major public health issue, characterized by a range of pathophysiological mechanisms and associated with life-long functional deficits for surviving patients and high socioeconomic costs for healthcare systems and societies. In search of efficient neuroregenerative treatments for this catastrophic disease, scientists have been studying various preclinical approaches, some of which have even reached the stage of clinical studies; however, a breakthrough has not been achieved in recent decades. The purpose of this Special Issue, thus, is to gather both original and clinical research articles, reviews, and perspectives to broaden our view on the field of neurotrauma and neuroregeneration, presenting approaches that have the potential to be translated into clinical practice. The subtopics of this issue include, but are not restricted to:

  1. Postinjury microenvironment changes, covering BBB (BSCB) disruption, neuroinflammation, and cellular survival.
  2. Neuropathic pain related to neuronal hyperexcitability, glutamate cytotoxicity, or chemokine release.
  3. Neural regeneration due to axonal regrowth, remyelination, circuit rewiring, or endogenous recruit.
  4. Novel therapeutic approaches including molecules, cells, noncellular organisms, gene therapies, biomaterials, or rehabilitative interventions. 

Dr. Alexander Younsi
Dr. Guoli Zheng
Dr. Xing Cheng
Guest Editors

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. Biology 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 2700 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

  • neurotrauma
  • spinal cord injury
  • traumatic brain injury
  • neuropathic pain
  • neuroinflammation
  • axonal regeneration
  • postinjury plasticity
  • neurorehabilitation
  • cell transplantation

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Published Papers (6 papers)

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Research

Jump to: Review

16 pages, 4243 KiB  
Article
Cofilin Inhibitor Protects against Traumatic Brain Injury-Induced Oxidative Stress and Neuroinflammation
by Ghaith A. Bahader, Antonisamy William James, Daniyah A. Almarghalani and Zahoor A. Shah
Biology 2023, 12(4), 630; https://doi.org/10.3390/biology12040630 - 21 Apr 2023
Cited by 11 | Viewed by 2863
Abstract
Microglial activation and failure of the antioxidant defense mechanisms are major hallmarks in different brain injuries, particularly traumatic brain injury (TBI). Cofilin is a cytoskeleton-associated protein involved in actin binding and severing. In our previous studies, we identified the putative role of cofilin [...] Read more.
Microglial activation and failure of the antioxidant defense mechanisms are major hallmarks in different brain injuries, particularly traumatic brain injury (TBI). Cofilin is a cytoskeleton-associated protein involved in actin binding and severing. In our previous studies, we identified the putative role of cofilin in mediating microglial activation and apoptosis in ischemic and hemorrhagic conditions. Others have highlighted the involvement of cofilin in ROS production and the resultant neuronal death; however, more studies are needed to delineate the role of cofilin in oxidative stress conditions. The present study aims to investigate the cellular and molecular effects of cofilin in TBI using both in vitro and in vivo models as well as the first-in-class small-molecule cofilin inhibitor (CI). An in vitro H2O2-induced oxidative stress model was used in two different types of cells, human neuroblastoma (SH-SY5Y) and microglia (HMC3), along with an in vivo controlled cortical impact model of TBI. Our results show that treatment with H2O2 increases the expression of cofilin and slingshot-1 (SSH-1), an upstream regulator of cofilin, in microglial cells, which was significantly reduced in the CI-treated group. Cofilin inhibition significantly attenuated H2O2-induced microglial activation by reducing the release of proinflammatory mediators. Furthermore, we demonstrate that CI protects against H2O2-induced ROS accumulation and neuronal cytotoxicity, activates the AKT signaling pathway by increasing its phosphorylation, and modulates mitochondrial-related apoptogenic factors. The expression of NF-E2-related factor 2 (Nrf2) and its associated antioxidant enzymes were also increased in CI-treated SY-SY5Y. In the mice model of TBI, CI significantly activated the Nrf2 and reduced the expression of oxidative/nitrosative stress markers at the protein and gene levels. Together, our data suggest that cofilin inhibition provides a neuroprotective effect in in vitro and in vivo TBI mice models by inhibiting oxidative stress and inflammatory responses, the pivotal mechanisms involved in TBI-induced brain damage. Full article
(This article belongs to the Special Issue Advances in the Fields of Neurotrauma and Neuroregeneration)
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11 pages, 2831 KiB  
Article
Abnormal Characterization and Distribution of Circulating Regulatory T Cells in Patients with Chronic Spinal Cord Injury According to the Period of Evolution
by Ana M. Gómez-Lahoz, Sergio Haro Girón, Jorge Monserrat Sanz, Oscar Fraile-Martínez, Cielo Garcia-Montero, Diego J. Jiménez, Diego de Leon-Oliva, Miguel A. Ortega, Mar Atienza-Perez, David Diaz, Elisa Lopez-Dolado and Melchor Álvarez-Mon
Biology 2023, 12(4), 617; https://doi.org/10.3390/biology12040617 - 19 Apr 2023
Cited by 2 | Viewed by 1378
Abstract
Spinal cord injury (SCI) is a progressive and complex neurological disorder accompanied by multiple systemic challenges. Peripheral immune dysfunction is a major event occurring after SCI, especially in its chronic phase. Previous works have demonstrated significant changes in different circulating immune compartments, including [...] Read more.
Spinal cord injury (SCI) is a progressive and complex neurological disorder accompanied by multiple systemic challenges. Peripheral immune dysfunction is a major event occurring after SCI, especially in its chronic phase. Previous works have demonstrated significant changes in different circulating immune compartments, including in T cells. However, the precise characterization of these cells remains to be fully unraveled, particularly when considering important variants such as the time since the initial injury. In the present work, we aimed to study the level of circulating regulatory T cells (Tregs) in SCI patients depending on the duration of evolution. For this purpose, we studied and characterized peripheral Tregs from 105 patients with chronic SCI using flow cytometry, with patients classified into three major groups depending on the time since initial injury: short period chronic (SCI-SP, <5 years since initial injury); early chronic (SCI-ECP, from 5–15 years post-injury) and late chronic SCI (SCI-LCP, more than 15 years post-injury. Our results show that both the SCI-ECP and SCI-LCP groups appeared to present increased proportions of CD4+ CD25+/low Foxp3+ Tregs in comparison to healthy subjects, whereas a decreased number of these cells expressing CCR5 was observed in SCI-SP, SCI-ECP, and SCI-LCP patients. Furthermore, an increased number of CD4+ CD25+/high/low Foxp3 with negative expression of CD45RA and CCR7 was observed in SCI-LCP patients when compared to the SCI-ECP group. Taken together, these results deepen our understanding of the immune dysfunction reported in chronic SCI patients and how the time since initial injury may drive this dysregulation. Full article
(This article belongs to the Special Issue Advances in the Fields of Neurotrauma and Neuroregeneration)
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Review

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20 pages, 1873 KiB  
Review
Axonal Regeneration after Spinal Cord Injury: Molecular Mechanisms, Regulatory Pathways, and Novel Strategies
by Mohammed Ibrahim Elmalky, Gonzalo Alvarez-Bolado, Alexander Younsi and Thomas Skutella
Biology 2024, 13(9), 703; https://doi.org/10.3390/biology13090703 - 7 Sep 2024
Viewed by 1988
Abstract
Axonal regeneration in the spinal cord after traumatic injuries presents a challenge for researchers, primarily due to the nature of adult neurons and the inhibitory environment that obstructs neuronal regrowth. Here, we review current knowledge of the intricate network of molecular and cellular [...] Read more.
Axonal regeneration in the spinal cord after traumatic injuries presents a challenge for researchers, primarily due to the nature of adult neurons and the inhibitory environment that obstructs neuronal regrowth. Here, we review current knowledge of the intricate network of molecular and cellular mechanisms that hinder axonal regeneration, with a focus on myelin-associated inhibitors (MAIs) and other inhibitory guidance molecules, as well as the pivotal pathways implicated in both inhibiting and facilitating axonal regrowth, such as PKA/AMP, PI3K/Akt/mTOR, and Trk, alongside the regulatory roles of neurotrophins and axonal guidance cues. We also examine current insights into gene therapy, tissue engineering, and pharmacological interventions that show promise in overcoming barriers to axonal regrowth. Full article
(This article belongs to the Special Issue Advances in the Fields of Neurotrauma and Neuroregeneration)
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29 pages, 2279 KiB  
Review
Biomaterials in Traumatic Brain Injury: Perspectives and Challenges
by Sarah Aqel, Najlaa Al-Thani, Mohammad Z. Haider, Samar Abdelhady, Asmaa A. Al Thani, Firas Kobeissy and Abdullah A. Shaito
Biology 2024, 13(1), 21; https://doi.org/10.3390/biology13010021 - 29 Dec 2023
Cited by 2 | Viewed by 3953
Abstract
Traumatic brain injury (TBI) is a leading cause of mortality and long-term impairment globally. TBI has a dynamic pathology, encompassing a variety of metabolic and molecular events that occur in two phases: primary and secondary. A forceful external blow to the brain initiates [...] Read more.
Traumatic brain injury (TBI) is a leading cause of mortality and long-term impairment globally. TBI has a dynamic pathology, encompassing a variety of metabolic and molecular events that occur in two phases: primary and secondary. A forceful external blow to the brain initiates the primary phase, followed by a secondary phase that involves the release of calcium ions (Ca2+) and the initiation of a cascade of inflammatory processes, including mitochondrial dysfunction, a rise in oxidative stress, activation of glial cells, and damage to the blood–brain barrier (BBB), resulting in paracellular leakage. Currently, there are no FDA-approved drugs for TBI, but existing approaches rely on delivering micro- and macromolecular treatments, which are constrained by the BBB, poor retention, off-target toxicity, and the complex pathology of TBI. Therefore, there is a demand for innovative and alternative therapeutics with effective delivery tactics for the diagnosis and treatment of TBI. Tissue engineering, which includes the use of biomaterials, is one such alternative approach. Biomaterials, such as hydrogels, including self-assembling peptides and electrospun nanofibers, can be used alone or in combination with neuronal stem cells to induce neurite outgrowth, the differentiation of human neural stem cells, and nerve gap bridging in TBI. This review examines the inclusion of biomaterials as potential treatments for TBI, including their types, synthesis, and mechanisms of action. This review also discusses the challenges faced by the use of biomaterials in TBI, including the development of biodegradable, biocompatible, and mechanically flexible biomaterials and, if combined with stem cells, the survival rate of the transplanted stem cells. A better understanding of the mechanisms and drawbacks of these novel therapeutic approaches will help to guide the design of future TBI therapies. Full article
(This article belongs to the Special Issue Advances in the Fields of Neurotrauma and Neuroregeneration)
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27 pages, 1683 KiB  
Review
Cellular and Molecular Pathophysiology of Traumatic Brain Injury: What Have We Learned So Far?
by Marco Aurelio M. Freire, Gabriel Sousa Rocha, Leonardo Oliveira Bittencourt, Daniel Falcao, Rafael Rodrigues Lima and Jose Rodolfo Lopes P. Cavalcanti
Biology 2023, 12(8), 1139; https://doi.org/10.3390/biology12081139 - 17 Aug 2023
Cited by 20 | Viewed by 8628
Abstract
Traumatic brain injury (TBI) is one of the leading causes of long-lasting morbidity and mortality worldwide, being a devastating condition related to the impairment of the nervous system after an external traumatic event resulting in transitory or permanent functional disability, with a significant [...] Read more.
Traumatic brain injury (TBI) is one of the leading causes of long-lasting morbidity and mortality worldwide, being a devastating condition related to the impairment of the nervous system after an external traumatic event resulting in transitory or permanent functional disability, with a significant burden to the healthcare system. Harmful events underlying TBI can be classified into two sequential stages, primary and secondary, which are both associated with breakdown of the tissue homeostasis due to impairment of the blood–brain barrier, osmotic imbalance, inflammatory processes, oxidative stress, excitotoxicity, and apoptotic cell death, ultimately resulting in a loss of tissue functionality. The present study provides an updated review concerning the roles of brain edema, inflammation, excitotoxicity, and oxidative stress on brain changes resulting from a TBI. The proper characterization of the phenomena resulting from TBI can contribute to the improvement of care, rehabilitation and quality of life of the affected people. Full article
(This article belongs to the Special Issue Advances in the Fields of Neurotrauma and Neuroregeneration)
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20 pages, 826 KiB  
Review
Multipotent Mesenchymal Stem Cell-Based Therapies for Spinal Cord Injury: Current Progress and Future Prospects
by Chih-Wei Zeng
Biology 2023, 12(5), 653; https://doi.org/10.3390/biology12050653 - 26 Apr 2023
Cited by 15 | Viewed by 4430
Abstract
Spinal cord injury (SCI) represents a significant medical challenge, often resulting in permanent disability and severely impacting the quality of life for affected individuals. Traditional treatment options remain limited, underscoring the need for novel therapeutic approaches. In recent years, multipotent mesenchymal stem cells [...] Read more.
Spinal cord injury (SCI) represents a significant medical challenge, often resulting in permanent disability and severely impacting the quality of life for affected individuals. Traditional treatment options remain limited, underscoring the need for novel therapeutic approaches. In recent years, multipotent mesenchymal stem cells (MSCs) have emerged as a promising candidate for SCI treatment due to their multifaceted regenerative capabilities. This comprehensive review synthesizes the current understanding of the molecular mechanisms underlying MSC-mediated tissue repair in SCI. Key mechanisms discussed include neuroprotection through the secretion of growth factors and cytokines, promotion of neuronal regeneration via MSC differentiation into neural cell types, angiogenesis through the release of pro-angiogenic factors, immunomodulation by modulating immune cell activity, axonal regeneration driven by neurotrophic factors, and glial scar reduction via modulation of extracellular matrix components. Additionally, the review examines the various clinical applications of MSCs in SCI treatment, such as direct cell transplantation into the injured spinal cord, tissue engineering using biomaterial scaffolds that support MSC survival and integration, and innovative cell-based therapies like MSC-derived exosomes, which possess regenerative and neuroprotective properties. As the field progresses, it is crucial to address the challenges associated with MSC-based therapies, including determining optimal sources, intervention timing, and delivery methods, as well as developing standardized protocols for MSC isolation, expansion, and characterization. Overcoming these challenges will facilitate the translation of preclinical findings into clinical practice, providing new hope and improved treatment options for individuals living with the devastating consequences of SCI. Full article
(This article belongs to the Special Issue Advances in the Fields of Neurotrauma and Neuroregeneration)
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