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Molecular and Physiological Mechanisms of Traumatic Brain Injury
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Molecular and Physiological Mechanisms of Traumatic Brain Injury

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: 30 June 2024 | Viewed by 2675

Special Issue Editor

Dr. Kwang Choi

E-Mail Website
Guest Editor
Department of Psychiatry, Uniformed Services University, Bethesda, MD, USA
Interests: substance use disorders; post-traumatic stress disorder; traumatic brain injury; neuroinflammation; ketamine; opioids; brain imaging; pain; major depressive disorder

Special Issue Information

Dear Colleagues,

Traumatic brain injury (TBI) affects millions of people every year and constitutes a critical public health problem with no consensus on evidence-based treatments. Although many patients with TBI may recover, a subset of individuals still suffer from long-lasting adverse effects such as physical, cognitive, emotional, social, and behavioural deficits. The primary brain injury is followed by a “secondary injury” caused by a cascade of pathological and biochemical changes. Specifically, cellular responses initiated by the primary injury are instigated in an attempt to restore homeostasis to the damaged tissue, but it often leads to exacerbation of the brain tissue damage, resulting in progressive neurodegeneration and cell death. For example, one of the common elements of secondary injury includes neuroinflammation, which contributes to functional deficits after TBI. While the primary brain injury is irreversible, the secondary injury may present an opportunity to discover pharmacological targets for TBI treatment.

We therefore invite academic and industrial investigators working in the fields of TBI to submit original research articles or reviews describing and discussing the molecular and biochemical mechanisms of TBI and progress in basic and clinical sciences related to TBI.

Potential topics include, but are not limited to:

  • Molecular and biochemical mechanisms of TBI;
  • Biomarkers including advanced neuroimaging and blood samples;
  • Novel interventions and treatment strategy;
  • Translational research to bridge gap between preclinical and clinical studies;
  • Comorbidity and mechanisms of TBI and neuropsychiatric disorders;
  • Mechanisms of sex-related differences in TBI.

Dr. Kwang Choi
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. 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.

Published Papers (4 papers)

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Research

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16 pages, 2022 KiB  
Article
Effects of Mild Closed-Head Injury and Subanesthetic Ketamine Infusion on Microglia, Axonal Injury, and Synaptic Density in Sprague–Dawley Rats
by Martin Boese, Rina Y. Berman, Jennifer Qiu, Haley F. Spencer, Kennett D. Radford and Kwang H. Choi
Int. J. Mol. Sci. 2024, 25(8), 4287; https://doi.org/10.3390/ijms25084287 - 12 Apr 2024
Viewed by 303
Abstract
Mild traumatic brain injury (mTBI) affects millions of people in the U.S. Approximately 20–30% of those individuals develop adverse symptoms lasting at least 3 months. In a rat mTBI study, the closed-head impact model of engineered rotational acceleration (CHIMERA) produced significant axonal injury [...] Read more.
Mild traumatic brain injury (mTBI) affects millions of people in the U.S. Approximately 20–30% of those individuals develop adverse symptoms lasting at least 3 months. In a rat mTBI study, the closed-head impact model of engineered rotational acceleration (CHIMERA) produced significant axonal injury in the optic tract (OT), indicating white-matter damage. Because retinal ganglion cells project to the lateral geniculate nucleus (LGN) in the thalamus through the OT, we hypothesized that synaptic density may be reduced in the LGN of rats following CHIMERA injury. A modified SEQUIN (synaptic evaluation and quantification by imaging nanostructure) method, combined with immunofluorescent double-labeling of pre-synaptic (synapsin) and post-synaptic (PSD-95) markers, was used to quantify synaptic density in the LGN. Microglial activation at the CHIMERA injury site was determined using Iba-1 immunohistochemistry. Additionally, the effects of ketamine, a potential neuroprotective drug, were evaluated in CHIMERA-induced mTBI. A single-session repetitive (ssr-) CHIMERA (3 impacts, 1.5 joule/impact) produced mild effects on microglial activation at the injury site, which was significantly enhanced by post-injury intravenous ketamine (10 mg/kg) infusion. However, ssr-CHIMERA did not alter synaptic density in the LGN, although ketamine produced a trend of reduction in synaptic density at post-injury day 4. Further research is necessary to characterize the effects of ssr-CHIMERA and subanesthetic doses of intravenous ketamine on different brain regions and multiple time points post-injury. The current study demonstrates the utility of the ssr-CHIMERA as a rodent model of mTBI, which researchers can use to identify biological mechanisms of mTBI and to develop improved treatment strategies for individuals suffering from head trauma. Full article
(This article belongs to the Special Issue Molecular and Physiological Mechanisms of Traumatic Brain Injury)
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13 pages, 1346 KiB  
Article
Establishing a 3-Tesla Magnetic Resonance Imaging Method for Assessing Diffuse Axonal Brain Injury in Rats
by Dmitry Frank, Benjamin F. Gruenbaum, Vladislav Zvenigorodsky, Ilan Shelef, Anna Oleshko, Frederic Matalon, Beatris Tsafarov, Alexander Zlotnik, Amit Frenkel and Matthew Boyko
Int. J. Mol. Sci. 2024, 25(8), 4234; https://doi.org/10.3390/ijms25084234 - 11 Apr 2024
Viewed by 333
Abstract
Traumatic brain injury (TBI) significantly contributes to death and disability worldwide. However, treatment options remain limited. Here, we focus on a specific pathology of TBI, diffuse axonal brain injury (DABI), which describes the process of the tearing of nerve fibers in the brain [...] Read more.
Traumatic brain injury (TBI) significantly contributes to death and disability worldwide. However, treatment options remain limited. Here, we focus on a specific pathology of TBI, diffuse axonal brain injury (DABI), which describes the process of the tearing of nerve fibers in the brain after blunt injury. Most protocols to study DABI do not incorporate a specific model for that type of pathology, limiting their ability to identify mechanisms and comorbidities of DABI. In this study, we developed a magnetic resonance imaging (MRI) protocol for DABI in a rat model using a 3-T clinical scanner. We compared the neuroimaging outcomes with histologic and neurologic assessments. In a sample size of 10 rats in the sham group and 10 rats in the DABI group, we established neurological severity scores before the intervention and at 48 h following DABI induction. After the neurological evaluation after DABI, all rats underwent MRI scans and were subsequently euthanized for histological evaluation. As expected, the neurological assessment showed a high sensitivity for DABI lesions indicated using the β-APP marker. Surprisingly, however, we found that the MRI method had greater sensitivity in assessing DABI lesions compared to histological methods. Out of the five MRI parameters with pathological changes in the DABI model, we found significant changes compared to sham rats in three parameters, and, as shown using comparative tests with other models, MRI was the most sensitive parameter, being even more sensitive than histology. We anticipate that this DABI protocol will have a significant impact on future TBI and DABI studies, advancing research on treatments specifically targeted towards improving patient quality of life and long-term outcomes. Full article
(This article belongs to the Special Issue Molecular and Physiological Mechanisms of Traumatic Brain Injury)
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15 pages, 4342 KiB  
Article
Traumatic Brain Injury Induces Nociceptin/Orphanin FQ and Nociceptin Opioid Peptide Receptor Expression within 24 Hours
by Omar N. Al Yacoub, Yong Zhang, Panini S. Patankar and Kelly M. Standifer
Int. J. Mol. Sci. 2024, 25(3), 1658; https://doi.org/10.3390/ijms25031658 - 29 Jan 2024
Viewed by 632
Abstract
Traumatic brain injury (TBI) is a major cause of mortality and disability around the world, for which no treatment has been found. Nociceptin/Orphanin FQ (N/OFQ) and the nociceptin opioid peptide (NOP) receptor are rapidly increased in response to fluid percussion, stab injury, and [...] Read more.
Traumatic brain injury (TBI) is a major cause of mortality and disability around the world, for which no treatment has been found. Nociceptin/Orphanin FQ (N/OFQ) and the nociceptin opioid peptide (NOP) receptor are rapidly increased in response to fluid percussion, stab injury, and controlled cortical impact (CCI) TBI. TBI-induced upregulation of N/OFQ contributes to cerebrovascular impairment, increased excitotoxicity, and neurobehavioral deficits. Our objective was to identify changes in N/OFQ and NOP receptor peptide, protein, and mRNA relative to the expression of injury markers and extracellular regulated kinase (ERK) 24 h following mild (mTBI) and moderate TBI (ModTBI) in wildtype (WT) and NOP receptor-knockout (KO) rats. N/OFQ was quantified by radioimmunoassay, mRNA expression was assessed using real-time PCR and protein levels were determined by immunoblot analysis. This study revealed increased N/OFQ mRNA and peptide levels in the CSF and ipsilateral tissue of WT, but not KO, rats 24 h post-TBI; NOP receptor mRNA increased after ModTBI. Cofilin-1 activation increased in the brain tissue of WT but not KO rats, ERK activation increased in all rats following ModTBI; no changes in injury marker levels were noted in brain tissue at this time. In conclusion, this study elucidates transcriptional and translational changes in the N/OFQ-NOP receptor system relative to TBI-induced neurological deficits and initiation of signaling cascades that support the investigation of the NOP receptor as a therapeutic target for TBI. Full article
(This article belongs to the Special Issue Molecular and Physiological Mechanisms of Traumatic Brain Injury)
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Review

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43 pages, 1317 KiB  
Review
Innovative Insights into Traumatic Brain Injuries: Biomarkers and New Pharmacological Targets
by Serena Silvestro, Ivana Raffaele, Angelo Quartarone and Emanuela Mazzon
Int. J. Mol. Sci. 2024, 25(4), 2372; https://doi.org/10.3390/ijms25042372 - 17 Feb 2024
Viewed by 1052
Abstract
A traumatic brain injury (TBI) is a major health issue affecting many people across the world, causing significant morbidity and mortality. TBIs often have long-lasting effects, disrupting daily life and functionality. They cause two types of damage to the brain: primary and secondary. [...] Read more.
A traumatic brain injury (TBI) is a major health issue affecting many people across the world, causing significant morbidity and mortality. TBIs often have long-lasting effects, disrupting daily life and functionality. They cause two types of damage to the brain: primary and secondary. Secondary damage is particularly critical as it involves complex processes unfolding after the initial injury. These processes can lead to cell damage and death in the brain. Understanding how these processes damage the brain is crucial for finding new treatments. This review examines a wide range of literature from 2021 to 2023, focusing on biomarkers and molecular mechanisms in TBIs to pinpoint therapeutic advancements. Baseline levels of biomarkers, including neurofilament light chain (NF-L), ubiquitin carboxy-terminal hydrolase-L1 (UCH-L1), Tau, and glial fibrillary acidic protein (GFAP) in TBI, have demonstrated prognostic value for cognitive outcomes, laying the groundwork for personalized treatment strategies. In terms of pharmacological progress, the most promising approaches currently target neuroinflammation, oxidative stress, and apoptotic mechanisms. Agents that can modulate these pathways offer the potential to reduce a TBI’s impact and aid in neurological rehabilitation. Future research is poised to refine these therapeutic approaches, potentially revolutionizing TBI treatment. Full article
(This article belongs to the Special Issue Molecular and Physiological Mechanisms of Traumatic Brain Injury)
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