Identifying Molecular or Cellular Level Pathomechanisms for Possible Therapeutic/Neuroprotective Interventions in Traumatic Brain Injury

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: 31 August 2024 | Viewed by 1114

Special Issue Editors


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Guest Editor
1. Szentágothai Research Center, University of Pecs, 7624 Pecs, Hungary
2. Department of Neurosurgery, Medical School, University of Pecs, 7623 Pecs, Hungary
Interests: traumatic brain injury (head injury): biomarkers; animal models; repetitive mild TBI; coagulopathy

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Guest Editor
1. Department of Neurosurgery, Medical School, University of Pecs, H-7623 Pecs, Hungary
2. Neurotrauma Research Group, Szentagothai Research Centre, University of Pecs, H-7624 Pecs, Hungary
3. ELKH-PTE Clinical Neuroscience MR Research Group, H-7623 Pecs, Hungary
Interests: traumatic brain injury (head injury); biomarkers; animal models; histopathological consequences; repetitive mild TBI; therapeutic (neuroprotective) interventions
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Special Issue Information

Dear Colleagues,

It is well known that traumatic brain injury represents a common clinical condition with a huge socio-economic burden. While, according to the data recently published by the Global Burden of Disease Study collaborators, there are more than 27 million new TBI cases estimated yearly worldwide associated with more than 8 million years of life lived with disability, other studies presume almost 70 thousand lethal cases in the USA and 75 thousand deaths, on top of about one million hospitalizations in Europe yearly, and all these numbers are still increasing.

Although the above-described data confirm the clear clinical need for causal (cellular level/neuroprotective) and, preferably, individualized therapeutic interventions—mainly due to the hypercomplex nature of possible pathological/pathophysiological sequelae induced by the head injury—so far (despite some clinical trials with controversial results with hypothermia, cyclosporine A and some steroid hormone analogues), there have been no real breakthroughs in this important field.

In light of the above, our current Special Issue is open to any clinical or experimental data related to any kind of promising neuroprotective interventions and/or revealed pathological alterations or pathophysiological processes which could serve as potential therapeutic targets in the near future.

Dr. Krisztina Amrein
Dr. Endre Czeiter
Guest Editors

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Keywords

  • traumatic brain injury
  • head injury
  • clinical study
  • experimental model
  • neuroprotective intervention
  • therapy
  • pathomechanism
  • molecular
  • cellular

Published Papers (1 paper)

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Research

22 pages, 5825 KiB  
Article
Valproic Acid Treatment after Traumatic Brain Injury in Mice Alleviates Neuronal Death and Inflammation in Association with Increased Plasma Lysophosphatidylcholines
by Regina Hummel, Erika Dorochow, Sonja Zander, Katharina Ritter, Lisa Hahnefeld, Robert Gurke, Irmgard Tegeder and Michael K. E. Schäfer
Cells 2024, 13(9), 734; https://doi.org/10.3390/cells13090734 - 23 Apr 2024
Viewed by 885
Abstract
The histone deacetylase inhibitor (HDACi) valproic acid (VPA) has neuroprotective and anti-inflammatory effects in experimental traumatic brain injury (TBI), which have been partially attributed to the epigenetic disinhibition of the transcription repressor RE1-Silencing Transcription Factor/Neuron-Restrictive Silencer Factor (REST/NRSF). Additionally, VPA changes post-traumatic brain [...] Read more.
The histone deacetylase inhibitor (HDACi) valproic acid (VPA) has neuroprotective and anti-inflammatory effects in experimental traumatic brain injury (TBI), which have been partially attributed to the epigenetic disinhibition of the transcription repressor RE1-Silencing Transcription Factor/Neuron-Restrictive Silencer Factor (REST/NRSF). Additionally, VPA changes post-traumatic brain injury (TBI) brain metabolism to create a neuroprotective environment. To address the interconnection of neuroprotection, metabolism, inflammation and REST/NRSF after TBI, we subjected C57BL/6N mice to experimental TBI and intraperitoneal VPA administration or vehicle solution at 15 min, 1, 2, and 3 days post-injury (dpi). At 7 dpi, TBI-induced an up-regulation of REST/NRSF gene expression and HDACi function of VPA on histone H3 acetylation were confirmed. Neurological deficits, brain lesion size, blood–brain barrier permeability, or astrogliosis were not affected, and REST/NRSF target genes were only marginally influenced by VPA. However, VPA attenuated structural damage in the hippocampus, microgliosis and expression of the pro-inflammatory marker genes. Analyses of plasma lipidomic and polar metabolomic patterns revealed that VPA treatment increased lysophosphatidylcholines (LPCs), which were inversely associated with interleukin 1 beta (Il1b) and tumor necrosis factor (Tnf) gene expression in the brain. The results show that VPA has mild neuroprotective and anti-inflammatory effects likely originating from favorable systemic metabolic changes resulting in increased plasma LPCs that are known to be actively taken up by the brain and function as carriers for neuroprotective polyunsaturated fatty acids. Full article
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