ijms-logo

Journal Browser

Journal Browser

Understanding Traumatic Brain Injury: Mechanisms and Therapeutic Targets 3.0

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 (30 November 2022) | Viewed by 10799

Special Issue 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,

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 is aimed 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 the head injured.

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
  • TBI
  • Neurotrauma
  • Translational research
  • Axonal injury
  • Neuroimaing
  • Apoptosis
  • Head
  • Biomarker

Related Special Issues

Published Papers (4 papers)

Order results
Result details
Select all
Export citation of selected articles as:

Research

Jump to: Review, Other

15 pages, 3575 KiB  
Article
Voluntary Exercise to Reduce Anxiety Behaviour in Traumatic Brain Injury Shown to Alleviate Inflammatory Brain Response in Mice
by Xiaoxuan Hu, Yuhang Ou, Jiashuo Li, Meiqi Sun, Qian Ge, Yongqi Pan, Zhenlu Cai, Ruolan Tan, Wenyu Wang, Jing An and Haixia Lu
Int. J. Mol. Sci. 2023, 24(7), 6365; https://doi.org/10.3390/ijms24076365 - 28 Mar 2023
Cited by 1 | Viewed by 1435
Abstract
Traumatic brain injury is a leading cause of neuroinflammation and anxiety disorders in young adults. Immune-targeted therapies have garnered attention for the amelioration of TBI-induced anxiety. A previous study has indicated that voluntary exercise intervention following TBI could reduce neuroinflammation. It is essential [...] Read more.
Traumatic brain injury is a leading cause of neuroinflammation and anxiety disorders in young adults. Immune-targeted therapies have garnered attention for the amelioration of TBI-induced anxiety. A previous study has indicated that voluntary exercise intervention following TBI could reduce neuroinflammation. It is essential to determine the effects of voluntary exercise after TBI on anxiety via inhibiting neuroinflammatory response. Mice were randomly divided into four groups (sham, TBI, sham + voluntary wheel running (VWR), and TBI + VWR). One-week VWR was carried out on the 2nd day after trauma. The neurofunction of TBI mice was assessed. Following VWR, anxiety behavior was evaluated, and neuroinflammatory responses in the perilesional cortex were investigated. Results showed that after one week of VWR, neurofunctional recovery was enhanced, while the anxiety behavior of TBI mice was significantly alleviated. The level of pro-inflammatory factors decreased, and the level of anti-inflammatory factors elevated. Activation of nucleotide oligomerization domain-like thermal receptor protein domain associated protein 3 (NLRP3) inflammasome was inhibited significantly. All these alterations were consistent with reduced microglial activation at the perilesional site and positively correlated with the amelioration of anxiety behavior. This suggested that timely rehabilitative exercise could be a useful therapeutic strategy for anxiety resulting from TBI by targeting neuroinflammation. Full article
Show Figures

Figure 1

17 pages, 4261 KiB  
Article
Neuroinflammation and Neuronal Loss in the Hippocampus Are Associated with Immediate Posttraumatic Seizures and Corticosterone Elevation in Rats
by Ilia G. Komoltsev, Stepan O. Frankevich, Natalia I. Shirobokova, Aleksandra A. Volkova, Mikhail V. Onufriev, Julia V. Moiseeva, Margarita R. Novikova and Natalia V. Gulyaeva
Int. J. Mol. Sci. 2021, 22(11), 5883; https://doi.org/10.3390/ijms22115883 - 30 May 2021
Cited by 16 | Viewed by 2787
Abstract
Hippocampal damage after traumatic brain injury (TBI) is associated with late posttraumatic conditions, such as depression, cognitive decline and epilepsy. Mechanisms of selective hippocampal damage after TBI are not well understood. In this study, using rat TBI model (lateral fluid percussion cortical injury), [...] Read more.
Hippocampal damage after traumatic brain injury (TBI) is associated with late posttraumatic conditions, such as depression, cognitive decline and epilepsy. Mechanisms of selective hippocampal damage after TBI are not well understood. In this study, using rat TBI model (lateral fluid percussion cortical injury), we assessed potential association of immediate posttraumatic seizures and changes in corticosterone (CS) levels with neuroinflammation and neuronal cell loss in the hippocampus. Indices of distant hippocampal damage (neurodegeneration and neuroinflammation) were assessed using histological analysis (Nissl staining, Iba-1 immunohistochemical staining) and ELISA (IL-1β and CS) 1, 3, 7 and 14 days after TBI or sham operation in male Wistar rats (n = 146). IL-1β was elevated only in the ipsilateral hippocampus on day 1 after trauma. CS peak was detected on day 3 in blood, the ipsilateral and contralateral hippocampus. Neuronal cell loss in the hippocampus was demonstrated bilaterally; in the ipsilateral hippocampus it started earlier than in the contralateral. Microglial activation was evident in the hippocampus bilaterally on day 7 after TBI. The duration of immediate seizures correlated with CS elevation, levels of IL-1β and neuronal loss in the hippocampus. The data suggest potential association of immediate post-traumatic seizures with CS-dependent neuroinflammation-mediated distant hippocampal damage. Full article
Show Figures

Figure 1

Review

Jump to: Research, Other

28 pages, 1106 KiB  
Review
The Role of BDNF in Experimental and Clinical Traumatic Brain Injury
by David Gustafsson, Andrea Klang, Sebastian Thams and Elham Rostami
Int. J. Mol. Sci. 2021, 22(7), 3582; https://doi.org/10.3390/ijms22073582 - 30 Mar 2021
Cited by 38 | Viewed by 4066
Abstract
Traumatic brain injury is one of the leading causes of mortality and morbidity in the world with no current pharmacological treatment. The role of BDNF in neural repair and regeneration is well established and has also been the focus of TBI research. Here, [...] Read more.
Traumatic brain injury is one of the leading causes of mortality and morbidity in the world with no current pharmacological treatment. The role of BDNF in neural repair and regeneration is well established and has also been the focus of TBI research. Here, we review experimental animal models assessing BDNF expression following injury as well as clinical studies in humans including the role of BDNF polymorphism in TBI. There is a large heterogeneity in experimental setups and hence the results with different regional and temporal changes in BDNF expression. Several studies have also assessed different interventions to affect the BDNF expression following injury. Clinical studies highlight the importance of BDNF polymorphism in the outcome and indicate a protective role of BDNF polymorphism following injury. Considering the possibility of affecting the BDNF pathway with available substances, we discuss future studies using transgenic mice as well as iPSC in order to understand the underlying mechanism of BDNF polymorphism in TBI and develop a possible pharmacological treatment. Full article
Show Figures

Figure 1

Other

Jump to: Research, Review

10 pages, 813 KiB  
Brief Report
Unilateral Cervical Vagotomy Modulates Immune Cell Profiles and the Response to a Traumatic Brain Injury
by M. Karen Newell-Rogers, Amanda Duong, Rizwan Nazarali, Richard P. Tobin, Susannah K. Rogers and Lee A. Shapiro
Int. J. Mol. Sci. 2022, 23(17), 9851; https://doi.org/10.3390/ijms23179851 - 30 Aug 2022
Cited by 1 | Viewed by 1678
Abstract
TBI induces splenic B and T cell expansion that contributes to neuroinflammation and neurodegeneration. The vagus nerve, the longest of the cranial nerves, is the predominant parasympathetic pathway allowing the central nervous system (CNS) control over peripheral organs, including regulation of inflammatory responses. [...] Read more.
TBI induces splenic B and T cell expansion that contributes to neuroinflammation and neurodegeneration. The vagus nerve, the longest of the cranial nerves, is the predominant parasympathetic pathway allowing the central nervous system (CNS) control over peripheral organs, including regulation of inflammatory responses. One way this is accomplished is by vagus innervation of the celiac ganglion, from which the splenic nerve innervates the spleen. This splenic innervation enables modulation of the splenic immune response, including splenocyte selection, activation, and downstream signaling. Considering that the left and right vagus nerves have distinct courses, it is possible that they differentially influence the splenic immune response following a CNS injury. To test this possibility, immune cell subsets were profiled and quantified following either a left or a right unilateral vagotomy. Both unilateral vagotomies caused similar effects with respect to the percentage of B cells and in the decreased percentage of macrophages and T cells following vagotomy. We next tested the hypothesis that a left unilateral vagotomy would modulate the splenic immune response to a traumatic brain injury (TBI). Mice received a left cervical vagotomy or a sham vagotomy 3 days prior to a fluid percussion injury (FPI), a well-characterized mouse model of TBI that consistently elicits an immune and neuroimmune response. Flow cytometric analysis showed that vagotomy prior to FPI resulted in fewer CLIP+ B cells, and CD4+, CD25+, and CD8+ T cells. Vagotomy followed by FPI also resulted in an altered distribution of CD11bhigh and CD11blow macrophages. Thus, transduction of immune signals from the CNS to the periphery via the vagus nerve can be targeted to modulate the immune response following TBI. Full article
Show Figures

Figure 1

Back to TopTop