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Understanding Traumatic Brain Injury: Mechanisms and Therapeutic Targets 2.0
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Understanding Traumatic Brain Injury: Mechanisms and Therapeutic Targets 2.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (28 February 2021) | Viewed by 23504

Special Issue Editor

Prof. András Büki

E-Mail Website
Guest Editor
Department of Neurosurgery, University Medical School, Pécs University, Pecs, Hungary
Interests: traumatic brain injury; brain injury biomarkers; advanced neuroimaging; translational research; neurotrauma models; transcortical magnetic stimulation
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue is the continuation of our previous successful Special Issue "Understanding Traumatic Brain Injury: Mechanisms and Therapeutic Targets".

It is currently appreciated that understanding the molecular mechanisms of traumatic brain injury is of ample importance to launch goal-driven, rationally targeted therapies. Thus far, despite promising developments in fundamental research, practically no clinical trials have proved effective in the treatment of traumatic brain injury. This has led to the recognition that our exploratory strategies should be revisited, and clinically relevant trauma models as well as translationally relevant endpoints should be established. This conclusion has materialized in the construction of the common data elements and the initiation of the Operation Brain Trauma Therapy program.

This Special Issue aims to summarize and coordinate thoughts, knowledge, and efforts to provide a better understanding of traumatic brain injury and open up new perspectives in bench-to-bedside approaches leading to a more efficient care for head injuries.

Specifically, we invite manuscripts focusing on molecular/pathobiological processes operant in various clinically relevant models of traumatic brain injury. We particularly encourage submission of reports on molecular, proteomic, metabolomic, and imaging markers of traumatically evoked brain injury, as well as studies of therapeutic interventions where target engagement is based on well-defined pathobiological processes with morphological, functional endpoints of translational relevance.

Prof. András Büki
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.

Keywords

  • Traumatic brain injury
  • Neurotrauma
  • Translational research
  • Axonal injury
  • Neuroimaing
  • Apoptosis
  • Biomarker

Related Special Issue

Published Papers (5 papers)

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Research

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17 pages, 2738 KiB  
Article
Potential Neuroprotective Mechanisms of Methamphetamine Treatment in Traumatic Brain Injury Defined by Large-Scale IonStar-Based Quantitative Proteomics
by Shichen Shen, Ming Zhang, Min Ma, Sailee Rasam, David Poulsen and Jun Qu
Int. J. Mol. Sci. 2021, 22(5), 2246; https://doi.org/10.3390/ijms22052246 - 24 Feb 2021
Cited by 4 | Viewed by 2615
Abstract
Although traumatic brain injury (TBI) causes hospitalizations and mortality worldwide, there are no approved neuroprotective treatments, partly due to a poor understanding of the molecular mechanisms underlying TBI neuropathology and neuroprotection. We previously reported that the administration of low-dose methamphetamine (MA) induced significant [...] Read more.
Although traumatic brain injury (TBI) causes hospitalizations and mortality worldwide, there are no approved neuroprotective treatments, partly due to a poor understanding of the molecular mechanisms underlying TBI neuropathology and neuroprotection. We previously reported that the administration of low-dose methamphetamine (MA) induced significant functional/cognitive improvements following severe TBI in rats. We further demonstrated that MA mediates neuroprotection in part, via dopamine-dependent activation of the PI3K-AKT pathway. Here, we further investigated the proteomic changes within the rat cortex and hippocampus following mild TBI (TM), severe TBI (TS), or severe TBI plus MA treatment (TSm) compared to sham operated controls. We identified 402 and 801 altered proteins (APs) with high confidence in cortical and hippocampal tissues, respectively. The overall profile of APs observed in TSm rats more closely resembled those seen in TM rather than TS rats. Pathway analysis suggested beneficial roles for acute signaling through IL-6, TGFβ, and IL-1β. Moreover, changes in fibrinogen levels observed in TSm rats suggested a potential role for these proteins in reducing/preventing TBI-induced coagulopathies. These data facilitate further investigations to identify specific pathways and proteins that may serve as key targets for the development of neuroprotective therapies. Full article
(This article belongs to the Special Issue Understanding Traumatic Brain Injury: Mechanisms and Therapeutic Targets 2.0)
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18 pages, 4416 KiB  
Article
Effects of Transient Receptor Potential Cation 5 (TRPC5) Inhibitor, NU6027, on Hippocampal Neuronal Death after Traumatic Brain Injury
by Min Kyu Park, Bo Young Choi, A Ra Kho, Song Hee Lee, Dae Ki Hong, Jeong Hyun Jeong, Dong Hyeon Kang, Beom Seok Kang and Sang Won Suh
Int. J. Mol. Sci. 2020, 21(21), 8256; https://doi.org/10.3390/ijms21218256 - 04 Nov 2020
Cited by 13 | Viewed by 2603
Abstract
Traumatic brain injury (TBI) can cause physical, cognitive, social, and behavioral changes that can lead to permanent disability or death. After primary brain injury, translocated free zinc can accumulate in neurons and lead to secondary events such as oxidative stress, inflammation, edema, swelling, [...] Read more.
Traumatic brain injury (TBI) can cause physical, cognitive, social, and behavioral changes that can lead to permanent disability or death. After primary brain injury, translocated free zinc can accumulate in neurons and lead to secondary events such as oxidative stress, inflammation, edema, swelling, and cognitive impairment. Under pathological conditions, such as ischemia and TBI, excessive zinc release, and accumulation occurs in neurons. Based on previous research, it hypothesized that calcium as well as zinc would be influx into the TRPC5 channel. Therefore, we hypothesized that the suppression of TRPC5 would prevent neuronal cell death by reducing the influx of zinc and calcium. To test our hypothesis, we used a TBI animal model. After the TBI, we immediately injected NU6027 (1 mg/kg, intraperitoneal), TRPC5 inhibitor, and then sacrificed animals 24 h later. We conducted Fluoro-Jade B (FJB) staining to confirm the presence of degenerating neurons in the hippocampal cornus ammonis 3 (CA3). After the TBI, the degenerating neuronal cell count was decreased in the NU6027-treated group compared with the vehicle-treated group. Our findings suggest that the suppression of TRPC5 can open a new therapeutic window for a reduction of the neuronal death that may occur after TBI. Full article
(This article belongs to the Special Issue Understanding Traumatic Brain Injury: Mechanisms and Therapeutic Targets 2.0)
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14 pages, 1974 KiB  
Article
Ethanol Intoxication Alleviates the Inflammatory Response of Remote Organs to Experimental Traumatic Brain Injury
by Baolin Xu, Akila Chandrasekar, Florian olde Heuvel, Maciej Powerski, Aleksander Nowak, Laurens Noack, Jazan Omari, Markus Huber-Lang, Francesco Roselli and Borna Relja
Int. J. Mol. Sci. 2020, 21(21), 8181; https://doi.org/10.3390/ijms21218181 - 31 Oct 2020
Cited by 8 | Viewed by 2980
Abstract
Traumatic brain injury (TBI) may cause damage to distant organs. Acute ethanol intoxication (EI) induces complex local and systemic anti-inflammatory effects and influences the early outcomes of traumatized patients. Here, we evaluated its effects on the BI-induced expression of local inflammatory mediators in [...] Read more.
Traumatic brain injury (TBI) may cause damage to distant organs. Acute ethanol intoxication (EI) induces complex local and systemic anti-inflammatory effects and influences the early outcomes of traumatized patients. Here, we evaluated its effects on the BI-induced expression of local inflammatory mediators in the trauma-remote organs the lungs and liver. Male mice were exposed to ethanol as a single oral dose (5g·kg–1, 32%) before inducing a moderate blunt TBI. Sham groups underwent the same procedures without TBI. Ether 3 or 6h after the TBI, the lung and liver were collected. The gene expression of HMGB1, IL-6, MMP9, IL-1β, and TNF as well as the homogenate protein levels of receptor for advanced glycation end products (RAGE), IL-6, IL-1β, and IL-10 were analyzed. Liver samples were immunohistologically stained for HMGB1. EI decreased the gene expressions of the proinflammatory markers HMGB1, IL-6, and MMP9 in the liver upon TBI. In line with the reduced gene expression, the TBI-induced protein expression of IL-6 in liver tissue homogenates was significantly reduced by EI at 3h after TBI. While the histological HMGB1 expression was enhanced by TBI, the RAGE protein expression in the liver tissue homogenates was diminished after TBI. EI reduced the histological HMGB1 expression and enhanced the hepatic RAGE protein expression at 6h post TBI. With regard to the lungs, EI significantly reduced the gene expressions of HMGB1, IL-6, IL-1β, and TNF upon TBI, without significantly affecting the protein expression levels of inflammatory markers (RAGE, IL-6, IL-1β, and IL-10). At the early stage of TBI-induced inflammation, the gene expression of inflammatory mediators in both the lungs and liver is susceptible to ethanol-induced remote effects. Taken together, EI may alleviate the TBI-induced pro-inflammatory response in the trauma-distant organs, the lungs and liver, via the HMGB1-RAGE axis. Full article
(This article belongs to the Special Issue Understanding Traumatic Brain Injury: Mechanisms and Therapeutic Targets 2.0)
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Review

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20 pages, 934 KiB  
Review
The Role of Estradiol in Traumatic Brain Injury: Mechanism and Treatment Potential
by Erzsébet Kövesdi, Edina Szabó-Meleg and István M. Abrahám
Int. J. Mol. Sci. 2021, 22(1), 11; https://doi.org/10.3390/ijms22010011 - 22 Dec 2020
Cited by 24 | Viewed by 3672
Abstract
Patients surviving traumatic brain injury (TBI) face numerous neurological and neuropsychological problems significantly affecting their quality of life. Extensive studies over the past decades have investigated pharmacological treatment options in different animal models, targeting various pathological consequences of TBI. Sex and gender are [...] Read more.
Patients surviving traumatic brain injury (TBI) face numerous neurological and neuropsychological problems significantly affecting their quality of life. Extensive studies over the past decades have investigated pharmacological treatment options in different animal models, targeting various pathological consequences of TBI. Sex and gender are known to influence the outcome of TBI in animal models and in patients, respectively. Apart from its well-known effects on reproduction, 17β-estradiol (E2) has a neuroprotective role in brain injury. Hence, in this review, we focus on the effect of E2 in TBI in humans and animals. First, we discuss the clinical classification and pathomechanism of TBI, the research in animal models, and the neuroprotective role of E2. Based on the results of animal studies and clinical trials, we discuss possible E2 targets from early to late events in the pathomechanism of TBI, including neuroinflammation and possible disturbances of the endocrine system. Finally, the potential relevance of selective estrogenic compounds in the treatment of TBI will be discussed. Full article
(This article belongs to the Special Issue Understanding Traumatic Brain Injury: Mechanisms and Therapeutic Targets 2.0)
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19 pages, 1364 KiB  
Review
Clinical Trials of Stem Cell Treatment for Spinal Cord Injury
by Kazuyoshi Yamazaki, Masahito Kawabori, Toshitaka Seki and Kiyohiro Houkin
Int. J. Mol. Sci. 2020, 21(11), 3994; https://doi.org/10.3390/ijms21113994 - 02 Jun 2020
Cited by 55 | Viewed by 10874
Abstract
There are more than one million patients worldwide suffering paralysis caused by spinal cord injury (SCI). SCI causes severe socioeconomic problems not only to the patients and their caregivers but also to society; therefore, the development of innovative treatments is crucial. Many pharmacological [...] Read more.
There are more than one million patients worldwide suffering paralysis caused by spinal cord injury (SCI). SCI causes severe socioeconomic problems not only to the patients and their caregivers but also to society; therefore, the development of innovative treatments is crucial. Many pharmacological therapies have been attempted in an effort to reduce SCI-related damage; however, no single therapy that could dramatically improve the serious long-term sequelae of SCI has emerged. Stem cell transplantation therapy, which can ameliorate damage or regenerate neurological networks, has been proposed as a promising candidate for SCI treatment, and many basic and clinical experiments using stem cells for SCI treatment have been launched, with promising results. However, the cell transplantation methods, including cell type, dose, transplantation route, and transplantation timing, vary widely between trials, and there is no consensus regarding the most effective treatment strategy. This study reviews the current knowledge on this issue, with a special focus on the clinical trials that have used stem cells for treating SCI, and highlights the problems that remain to be solved before the widespread clinical use of stem cells can be adopted. Full article
(This article belongs to the Special Issue Understanding Traumatic Brain Injury: Mechanisms and Therapeutic Targets 2.0)
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