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Cellular and Molecular Mechanisms of Traumatic Brain Injury and Concussion
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Cellular and Molecular Mechanisms of Traumatic Brain Injury and Concussion

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: closed (30 April 2022) | Viewed by 14754

Special Issue Editor

Dr. Changiz Taghibiglou

E-Mail Website
Guest Editor
Department of Anatomy, Physiology, Pharmacology, University of Saskatchewan, Saskatoon, SK, Canada
Interests: concussion; traumatic brain injury; stroke; biomarkers; excitotoxicity; lipid rafts; srebps; neurodegenrative diseases

Special Issue Information

Dear Colleagues,

Traumatic brain injury (TBI)/concussion is usually the result of an external force causing rapid acceleration and/or decelerations of the head, leading to the disruption of normal brain functions. TBI is a growing epidemic throughout the world and is considered a leading cause of disability and mortality, particularly among those younger than 45. More than 69 million individuals suffer from TBI worldwide annually. The leading causes of TBI include vehicle accidents, falls, assaults, sports-related injuries, and injuries sustained during military operations. There are two phases of injuries in TBI: the primary phase (instantaneous insult/injury) caused by the external forces; and the secondary phase (delayed or functional injury) sustained by molecular injuries which add more complexity and unpredictability/variability for short- and long-term patient management and treatment. 

A wide variety of cellular and molecular mechanisms have been identified contributing to the pathogenesis of TBI. A better understanding of the pathophysiology behind TBI is essential for providing more effective treatment. The majority of neuronal death and loss often occurs in the second phase of TBI. Various detrimental processes, including inflammation, ischemia, free radical formation/oxidative stress, and excitotoxicity, are involved in the overall pathobiology of TBI.

Considering the high occurrence of TBI and its severe short- and long-term health consequences, a better understanding of underlying molecular mechanisms will definitely assist us in finding more effective diagnostic (biomarkers) tools and therapeutic interventions.

Therefore, the focus of this Special Issue of the International Journal of Molecular Sciences (IJMS) is dedicated to research and review articles to cover the latest progress in understanding molecular and cellular mechanisms of traumatic brain injury and concussion, as well as diagnostic, preventive, and therapeutic approaches for TBI.

Dr. Changiz Taghibiglou
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

  • concussion
  • traumatic brain injury
  • biomarkers
  • excitotoxicity
  • neurodegenrative diseases

Published Papers (4 papers)

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Research

16 pages, 5002 KiB  
Article
Concussion/Mild Traumatic Brain Injury (TBI) Induces Brain Insulin Resistance: A Positron Emission Tomography (PET) Scanning Study
by Sathiya Sekar, Raja Solomon Viswas, Hajar Miranzadeh Mahabadi, Elahe Alizadeh, Humphrey Fonge and Changiz Taghibiglou
Int. J. Mol. Sci. 2021, 22(16), 9005; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22169005 - 20 Aug 2021
Cited by 6 | Viewed by 2498
Abstract
Brain injury/concussion is a growing epidemic throughout the world. Although evidence supports association between traumatic brain injury (TBI) and disturbance in brain glucose metabolism, the underlying molecular mechanisms are not well established. Previously, we reported the release of cellular prion protein (PrPc) from [...] Read more.
Brain injury/concussion is a growing epidemic throughout the world. Although evidence supports association between traumatic brain injury (TBI) and disturbance in brain glucose metabolism, the underlying molecular mechanisms are not well established. Previously, we reported the release of cellular prion protein (PrPc) from the brain to circulation following TBI. The PrPc level was also found to be decreased in insulin-resistant rat brains. In the present study, we investigated the molecular link between PrPc and brain insulin resistance in a single and repeated mild TBI-induced mouse model. Mild TBI was induced in mice by dropping a weight (~95 g at 1 m high) on the right side of the head. The procedure was performed once and thrice (once daily) for single (SI) and repeated induction (RI), respectively. Micro PET/CT imaging revealed that RI mice showed significant reduction in cortical, hippocampal and cerebellum glucose uptake compared to SI and control. Mice that received RI also showed significant motor and cognitive deficits. In co-immunoprecipitation, the interaction between PrPc, flotillin and Cbl-associated protein (CAP) observed in the control mice brains was disrupted by RI. Lipid raft isolation showed decreased levels of PrPc, flotillin and CAP in the RI mice brains. Based on observation, it is clear that PrPc has an interaction with CAP and the dislodgment of PrPc from cell membranes may lead to brain insulin resistance in a mild TBI mouse model. The present study generated a new insight into the pathogenesis of brain injury, which may result in the development of novel therapy. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms of Traumatic Brain Injury and Concussion)
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18 pages, 2161 KiB  
Article
Lack of Glutamate Receptor Subunit Expression Changes in Hippocampal Dentate Gyrus after Experimental Traumatic Brain Injury in a Rodent Model of Depression
by Maxon V. Knott, Laura B. Ngwenya, Erika A. Correll, Judy Bohnert, Noah J. Ziemba, Emily Allgire, Tracy Hopkins and Jennifer L. McGuire
Int. J. Mol. Sci. 2021, 22(15), 8086; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22158086 - 28 Jul 2021
Cited by 3 | Viewed by 2158
Abstract
Traumatic brain injury (TBI) affects over 69 million people annually worldwide, and those with pre-existing depression have worse recovery. The molecular mechanisms that may contribute to poor recovery after TBI with co-morbid depression have not been established. TBI and depression have many commonalities [...] Read more.
Traumatic brain injury (TBI) affects over 69 million people annually worldwide, and those with pre-existing depression have worse recovery. The molecular mechanisms that may contribute to poor recovery after TBI with co-morbid depression have not been established. TBI and depression have many commonalities including volume changes, myelin disruption, changes in proliferation, and changes in glutamatergic signaling. We used a well-established animal model of depression, the Wistar Kyoto (WKY) rat, to elucidate changes after TBI that may influence the recovery trajectory. We compared the histological and molecular outcomes in the hippocampal dentate gyrus after experimental TBI using the lateral fluid percussion injury (LFPI) in the WKY and the parent Wistar (WIS) strain. We showed that WKY had exaggerated myelin loss after LFPI and baseline deficits in proliferation. In addition, we showed that while after LFPI WIS rats exhibited glutamate receptor subunit changes, namely increased GluN2B, the WKY rats failed to show such injury-related changes. These differential responses to LFPI helped to elucidate the molecular characteristics that influence poor recovery after TBI in those with pre-existing depression and may lead to targets for future therapeutic interventions. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms of Traumatic Brain Injury and Concussion)
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27 pages, 3405 KiB  
Article
Plasma miR-9-3p and miR-136-3p as Potential Novel Diagnostic Biomarkers for Experimental and Human Mild Traumatic Brain Injury
by Shalini Das Gupta, Robert Ciszek, Mette Heiskanen, Niina Lapinlampi, Janne Kukkonen, Ville Leinonen, Noora Puhakka and Asla Pitkänen
Int. J. Mol. Sci. 2021, 22(4), 1563; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22041563 - 04 Feb 2021
Cited by 21 | Viewed by 5434
Abstract
Noninvasive, affordable circulating biomarkers for difficult-to-diagnose mild traumatic brain injury (mTBI) are an unmet medical need. Although blood microRNA (miRNA) levels are reportedly altered after traumatic brain injury (TBI), their diagnostic potential for mTBI remains inconclusive. We hypothesized that acutely altered plasma miRNAs [...] Read more.
Noninvasive, affordable circulating biomarkers for difficult-to-diagnose mild traumatic brain injury (mTBI) are an unmet medical need. Although blood microRNA (miRNA) levels are reportedly altered after traumatic brain injury (TBI), their diagnostic potential for mTBI remains inconclusive. We hypothesized that acutely altered plasma miRNAs could serve as diagnostic biomarkers both in the lateral fluid percussion injury (FPI) model and clinical mTBI. We performed plasma small RNA-sequencing from adult male Sprague–Dawley rats (n = 31) at 2 days post-TBI, followed by polymerase chain reaction (PCR)-based validation of selected candidates. miR-9a-3p, miR-136-3p, and miR-434-3p were identified as the most promising candidates at 2 days after lateral FPI. Digital droplet PCR (ddPCR) revealed 4.2-, 2.8-, and 4.6-fold elevations in miR-9a-3p, miR-136-3p, and miR-434-3p levels (p < 0.01 for all), respectively, distinguishing rats with mTBI from naïve rats with 100% sensitivity and specificity. DdPCR further identified a subpopulation of mTBI patients with plasma miR-9-3p (n = 7/15) and miR-136-3p (n = 5/15) levels higher than one standard deviation above the control mean at <2 days postinjury. In sTBI patients, plasma miR-9-3p levels were 6.5- and 9.2-fold in comparison to the mTBI and control groups, respectively. Thus, plasma miR-9-3p and miR-136-3p were identified as promising biomarker candidates for mTBI requiring further evaluation in a larger patient population. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms of Traumatic Brain Injury and Concussion)
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14 pages, 3956 KiB  
Article
Repetitive Traumatic Brain Injury Causes Neuroinflammation before Tau Pathology in Adolescent P301S Mice
by Saef Izzy, Alexander Brown-Whalen, Taha Yahya, Aliyah Sarro-Schwartz, Gina Jin, Joon Yong Chung, Sevda Lule, Liza M. Morsett, Ali Alquraini, Limin Wu, Suzanne E. Hickman, Michael J. Whalen and Joseph El Khoury
Int. J. Mol. Sci. 2021, 22(2), 907; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22020907 - 18 Jan 2021
Cited by 9 | Viewed by 3309
Abstract
Repetitive closed head injury (rCHI) is commonly encountered in young athletes engaged in contact and collision sports. Traumatic brain injury (TBI) including rCHI has been reported to be an important risk factor for several tauopathies in studies of adult humans and animals. However, [...] Read more.
Repetitive closed head injury (rCHI) is commonly encountered in young athletes engaged in contact and collision sports. Traumatic brain injury (TBI) including rCHI has been reported to be an important risk factor for several tauopathies in studies of adult humans and animals. However, the link between rCHI and the progression of tau pathology in adolescents remains to be elucidated. We evaluated whether rCHI can trigger the initial acceleration of pathological tau in adolescent mice and impact the long-term outcomes post-injury. To this end, we subjected adolescent transgenic mice expressing the P301S tau mutation to mild rCHI and assessed tau hyperphosphorylation, tangle formation, markers of neuroinflammation, and behavioral deficits at 40 days post rCHI. We report that rCHI did not accelerate tau pathology and did not worsen behavioral outcomes compared to control mice. However, rCHI induced cortical and hippocampal microgliosis and corpus callosum astrocytosis in P301S mice by 40 days post-injury. In contrast, we did not find significant microgliosis or astrocytosis after rCHI in age-matched WT mice or sham-injured P301S mice. Our data suggest that neuroinflammation precedes the development of Tau pathology in this rCHI model of adolescent repetitive mild TBI. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms of Traumatic Brain Injury and Concussion)
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