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Molecular Research on Brain Injury
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Molecular Research on 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: closed (31 August 2023) | Viewed by 7122

Special Issue Editors

Dr. Ann M. Marini

E-Mail Website
Guest Editor
Department of Neurology, Uniformed Services University of the Health Sciences, Bethesda, MD, USA
Interests: brain injury; neuroprotection; nutraceuticals
Dr. Maria Fatima M. Braga

E-Mail Website
Guest Editor
1. Department of Anatomy, Physiology, and Genetics, F. Edward Hébert School of Medicine, Uniformed Services University of the Health Sciences, Bethesda, MD, USA
2. Department of Psychiatry, F. Edward Hébert School of Medicine, Uniformed Services University of the Health Sciences, Bethesda, MD, USA
Interests: brain injury; epilepsy; neurodegeneration

Special Issue Information

Dear Colleagues,

Injuries to the brain can happen in many ways and are classified into two main categories: traumatic and non-traumatic. Non-traumatic brain injuries can be caused by a variety of conditions including strokes, metabolic disorders, tumors, aneurysms, prolonged seizures, cardiac arrest, oxygen deprivation, and toxins, to name a few. In contrast to a traumatic brain injury (TBI), these injuries are not the result of an external physical force that impacts or penetrates the head. Nonetheless, the short- and long-term effects of a non-traumatic brain injury (non-TBI) occur as they do after a TBI. A closed head injury TBI, an injury to the brain caused by an external force, can be classified as mild, moderate or severe. TBIs can also be classified based on the mechanism that caused it, as a closed or penetrating head injury, or as a blast-induced TBI. Brain injuries disrupt the normal flow of complex communications and interactions between cells in the brain. The impacts of these injuries result in neurological deficits. These deficits involve motor, sensory, cognitive and/or emotional components. Numerous researchers have used molecular biology and electrophysiological methods to investigate the pathophysiological alterations that occur in the brain’s neuronal circuits that compromise function after injury. This open access Special Issue will bring together new research and review articles on molecular biological and electrophysiological mechanisms that alter normal brain function after brain injury. Delineating the molecular and electrophysiological mechanisms of the cells and environment surrounding the injury, and developing treatments using current molecular tools, including single-cell sequencing, will advance our understanding of the complex interactions and lead to the restoration of normal brain function. These results may lead to the discovery of new molecular diagnostics, novel therapeutic targets, and better outcomes.

Topics of interest for this Special Issue include:

  • Closed traumatic brain injury;
  • Penetrating traumatic brain injury;
  • Chronic traumatic encephalopathy;
  • Blast-induced traumatic brain injury;
  • Ischemic stroke;
  • Hemorrhagic stroke;
  • Status epilepticus;
  • Meningitis;
  • COVID-19-related brain injury;
  • AIDS-related brain injury;
  • Toxin-induced brain injury;
  • Multiple-sclerosis-induced brain injury;
  • Therapeutics on the horizon for brain injuries.

Dr. Ann M. Marini
Dr. Maria Fatima M. Braga
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. 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

  • brain injury
  • stroke
  • chronic traumatic encephalopathy
  • status epilepticus
  • oxygen deprivation
  • metabolic disorders
  • tumors
  • aneurysms
  • prolonged seizures
  • cardiac arrest
  • oxygen deprivation
  • meningitis
  • COVID-19 brain injury
  • AIDS-related brain injury
  • toxin-induced brain injury
  • multiple-sclerosis-induced brain injury

Published Papers (4 papers)

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Research

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32 pages, 5810 KiB  
Article
Treatment of Status Epilepticus after Traumatic Brain Injury Using an Antiseizure Drug Combined with a Tissue Recovery Enhancer Revealed by Systems Biology
by Natallie Kajevu, Anssi Lipponen, Pedro Andrade, Ivette Bañuelos, Noora Puhakka, Elina Hämäläinen, Teemu Natunen, Mikko Hiltunen and Asla Pitkänen
Int. J. Mol. Sci. 2023, 24(18), 14049; https://doi.org/10.3390/ijms241814049 - 13 Sep 2023
Cited by 1 | Viewed by 1119
Abstract
We tested a hypothesis that in silico-discovered compounds targeting traumatic brain injury (TBI)-induced transcriptomics dysregulations will mitigate TBI-induced molecular pathology and augment the effect of co-administered antiseizure treatment, thereby alleviating functional impairment. In silico bioinformatic analysis revealed five compounds substantially affecting TBI-induced transcriptomics [...] Read more.
We tested a hypothesis that in silico-discovered compounds targeting traumatic brain injury (TBI)-induced transcriptomics dysregulations will mitigate TBI-induced molecular pathology and augment the effect of co-administered antiseizure treatment, thereby alleviating functional impairment. In silico bioinformatic analysis revealed five compounds substantially affecting TBI-induced transcriptomics regulation, including calpain inhibitor, chlorpromazine, geldanamycin, tranylcypromine, and trichostatin A (TSA). In vitro exposure of neuronal-BV2-microglial co-cultures to compounds revealed that TSA had the best overall neuroprotective, antioxidative, and anti-inflammatory effects. In vivo assessment in a rat TBI model revealed that TSA as a monotherapy (1 mg/kg/d) or in combination with the antiseizure drug levetiracetam (LEV 150 mg/kg/d) mildly mitigated the increase in plasma levels of the neurofilament subunit pNF-H and cortical lesion area. The percentage of rats with seizures during 0–72 h post-injury was reduced in the following order: TBI-vehicle 80%, TBI-TSA (1 mg/kg) 86%, TBI-LEV (54 mg/kg) 50%, TBI-LEV (150 mg/kg) 40% (p < 0.05 vs. TBI-vehicle), and TBI-LEV (150 mg/kg) combined with TSA (1 mg/kg) 30% (p < 0.05). Cumulative seizure duration was reduced in the following order: TBI-vehicle 727 ± 688 s, TBI-TSA 898 ± 937 s, TBI-LEV (54 mg/kg) 358 ± 715 s, TBI-LEV (150 mg/kg) 42 ± 64 (p < 0.05 vs. TBI-vehicle), and TBI-LEV (150 mg/kg) combined with TSA (1 mg/kg) 109 ± 282 s (p < 0.05). This first preclinical intervention study on post-TBI acute seizures shows that a combination therapy with the tissue recovery enhancer TSA and LEV was safe but exhibited no clear benefit over LEV monotherapy on antiseizure efficacy. A longer follow-up is needed to confirm the possible beneficial effects of LEV monotherapy and combination therapy with TSA on chronic post-TBI structural and functional outcomes, including epileptogenesis. Full article
(This article belongs to the Special Issue Molecular Research on Brain Injury)
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17 pages, 1939 KiB  
Article
Preliminary Development of a Brainwave Model for K1 Kickboxers Using Quantitative Electroencephalography (QEEG) with Open Eyes
by Łukasz Rydzik, Tadeusz Ambroży, Tomasz Pałka, Wojciech Wąsacz, Michał Spieszny, Jacek Perliński, Paweł Król and Marta Kopańska
Int. J. Mol. Sci. 2023, 24(10), 8882; https://doi.org/10.3390/ijms24108882 - 17 May 2023
Cited by 5 | Viewed by 1209
Abstract
K1 kickboxing fighting is characterised by high injury rates due to the low restrictions of fighting rules. In recent years, much attention has been paid to research on changes in brain function among athletes, including those in combat sports. One of the tools [...] Read more.
K1 kickboxing fighting is characterised by high injury rates due to the low restrictions of fighting rules. In recent years, much attention has been paid to research on changes in brain function among athletes, including those in combat sports. One of the tools that are likely to help diagnose and assess brain function is quantitative electroencephalography (QEEG). Therefore, the aim of the present study was an attempt to develop a brainwave model using quantitative electroencephalography in competitive K1 kickboxers. A total of thirty-six male individuals were purposefully selected and then comparatively divided into two groups. The first group consisted of specialised K1 kickboxing athletes exhibiting a high level of sports performance (experimental group, n = 18, mean age: 29.83 ± 3.43), while the second group comprised healthy individuals not training competitively (control group, n = 18, mean age: 26.72 ± 1.77). Body composition assessment was performed in all participants before the main measurement process. Measurements were taken for kickboxers during the de-training period, after the sports competition phase. Quantitative electroencephalography of Delta, Theta, Alpha, sensimotor rhytm (SMR), Beta1 and Beta2 waves was performed using electrodes placed on nine measurement points (frontal: FzF3F4, central: CzC3C4, and parietal: PzP3P4) with open eyes. In the course of the analyses, it was found that the level of brain activity among the study population significantly differentiated the K1 formula competitors compared with the reference standards and the control group in selected measurement areas. For kickboxers, all results of the Delta amplitude activity in the area of the frontal lobe were significantly above the normative values for this wave. The highest value was recorded for the average value of the F3 electrode (left frontal lobe), exceeding the norm by 95.65%, for F4 by 74.45% and Fz by 50.6%, respectively. In addition, the Alpha wave standard value for the F4 electrode was exceeded by 14.6%. Normative values were found for the remaining wave amplitudes. Statistically significant differentiation of results, with a strong effect (d = 1.52–8.41), was shown for the activity of Delta waves of the frontal area and the central part of the parietal area (Fz,F3,F4,Cz—p < 0.001), Theta for the frontal area as well as the central and left parietal lobes (Fz,F3,F4—p < 0.001, Cz—p = 0.001, C3—p = 0.018; d = 1.05–3.18), Alpha for the frontal, parietal and occipital areas (for: Fz,F3—p < 0.001, F4—p = 0.036, Cz—p < 0.001, C3—p = 0.001, C4—p = 0.025, Pz—p = 0.010, P3—p < 0.001, P4—p = 0.038; d = 0.90–1.66), SMR for the central parietal and left occipital lobes (Cz—p = 0.043; d = 0.69, P3—p < 0.001; d = 1.62), Beta for the frontal area, occipital and central lobes and left parietal segment (Fz,F3—p < 0.001, F4—p = 0.008, Cz, C3, Pz, P3,P4—p < 0.001; d = 1.27–2.85) and Beta 2 for all measurement areas (Fz, F3, F4, Cz, C3, C4, Pz, P3, P4—p < 0.001; d = 1.90–3.35) among the study groups. Significantly higher results were shown in the kickboxer group compared to the control. In addition to problems with concentration or over-stimulation of neural structures, high Delta waves, with elevated Alpha, Theta and Beta 2 waves, can cause disorders in the limbic system and problems in the cerebral cortex. Full article
(This article belongs to the Special Issue Molecular Research on Brain Injury)
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17 pages, 2780 KiB  
Article
Dexmedetomidine Protects Cerebellar Neurons against Hyperoxia-Induced Oxidative Stress and Apoptosis in the Juvenile Rat
by Robert Puls, Clarissa von Haefen, Christoph Bührer and Stefanie Endesfelder
Int. J. Mol. Sci. 2023, 24(9), 7804; https://doi.org/10.3390/ijms24097804 - 25 Apr 2023
Cited by 2 | Viewed by 1405
Abstract
The risk of oxidative stress is unavoidable in preterm infants and increases the risk of neonatal morbidities. Premature infants often require sedation and analgesia, and the commonly used opioids and benzodiazepines are associated with adverse effects. Impairment of cerebellar functions during cognitive development [...] Read more.
The risk of oxidative stress is unavoidable in preterm infants and increases the risk of neonatal morbidities. Premature infants often require sedation and analgesia, and the commonly used opioids and benzodiazepines are associated with adverse effects. Impairment of cerebellar functions during cognitive development could be a crucial factor in neurodevelopmental disorders of prematurity. Recent studies have focused on dexmedetomidine (DEX), which has been associated with potential neuroprotective properties and is used as an off-label application in neonatal units. Wistar rats (P6) were exposed to 80% hyperoxia for 24 h and received as pretreatment a single dose of DEX (5µg/kg, i.p.). Analyses in the immature rat cerebellum immediately after hyperoxia (P7) and after recovery to room air (P9, P11, and P14) included examinations for cell death and inflammatory and oxidative responses. Acute exposure to high oxygen concentrations caused a significant oxidative stress response, with a return to normal levels by P14. A marked reduction of hyperoxia-mediated damage was demonstrated after DEX pretreatment. DEX produced a much earlier recovery than in controls, confirming a neuroprotective effect of DEX on alterations elicited by oxygen stress on the developing cerebellum. Full article
(This article belongs to the Special Issue Molecular Research on Brain Injury)
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Review

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20 pages, 1543 KiB  
Review
Succinyl-CoA Synthetase Dysfunction as a Mechanism of Mitochondrial Encephalomyopathy: More than Just an Oxidative Energy Deficit
by Makayla S. Lancaster and Brett H. Graham
Int. J. Mol. Sci. 2023, 24(13), 10725; https://doi.org/10.3390/ijms241310725 - 27 Jun 2023
Cited by 4 | Viewed by 2716
Abstract
Biallelic pathogenic variants in subunits of succinyl-CoA synthetase (SCS), a tricarboxylic acid (TCA) cycle enzyme, are associated with mitochondrial encephalomyopathy in humans. SCS catalyzes the interconversion of succinyl-CoA to succinate, coupled to substrate-level phosphorylation of either ADP or GDP, within the TCA cycle. [...] Read more.
Biallelic pathogenic variants in subunits of succinyl-CoA synthetase (SCS), a tricarboxylic acid (TCA) cycle enzyme, are associated with mitochondrial encephalomyopathy in humans. SCS catalyzes the interconversion of succinyl-CoA to succinate, coupled to substrate-level phosphorylation of either ADP or GDP, within the TCA cycle. SCS-deficient encephalomyopathy typically presents in infancy and early childhood, with many patients succumbing to the disease during childhood. Common symptoms include abnormal brain MRI, basal ganglia lesions and cerebral atrophy, severe hypotonia, dystonia, progressive psychomotor regression, and growth deficits. Although subunits of SCS were first identified as causal genes for progressive metabolic encephalomyopathy in the early 2000s, recent investigations are now beginning to unravel the pathomechanisms underlying this metabolic disorder. This article reviews the current understanding of SCS function within and outside the TCA cycle as it relates to the complex and multifactorial mechanisms underlying SCS-related mitochondrial encephalomyopathy. Full article
(This article belongs to the Special Issue Molecular Research on Brain Injury)
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