Emerging Trends in Traumatic Brain Injury

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: closed (30 April 2025) | Viewed by 1580

Special Issue Editor


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Guest Editor
1. Department of Neurosurgery, University Hospitals Birmingham, Edgbaston, Birmingham, UK
2. Institute of Inflammation and Ageing, University of Birmingham, Edgbaston, Birmingham, UK
Interests: photonic approaches to the central nervous system; NIRS; Raman; LLLT; cold laser therapy; brain biomarkers; concussion and mild TBI; severe TBI

Special Issue Information

Dear Colleagues,

Optical spectroscopic and therapeutic approaches to the brain and central nervous system are continuing to evolve and represent a novel and exciting modality for both monitoring the development of pathology and modifying the disease process directly. Near infrared spectroscopy (NIRS) has developed significantly in complexity as a mode of measuring oxidative metabolism and haemodynamics both invasively and non-invasively in a range of neurological disorders. The potential that light within the NIR spectrum can potentially reduce the burden of cell loss within the acute phase of injury and effect ongoing function after traumatic brain injury has been speculated in multiple publications in the past. Quality publications are slowly evolving to this effect; however, having been honoured with this invitation as guest editor, I would like to use this opportunity to focus on and strengthen the evidence base around this exciting topic. 

I would like to encourage focus, develop ideas, and encourage submissions from colleagues on the fundamental interaction between light and the brain in terms of both monitoring and intervention within the context of the pathology of traumatic brain injury.

Dr. David James Davies
Guest Editor

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Keywords

  • photonic approaches to the central nervous system
  • NIRS
  • Raman
  • LLLT
  • cold laser therapy
  • brain biomarkers
  • concussion and mild TBI
  • severe TBI

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Published Papers (1 paper)

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Research

17 pages, 5155 KiB  
Article
Neuroprotective Effects of Functionalized Hydrophilic Carbon Clusters: Targeted Therapy of Traumatic Brain Injury in an Open Blast Rat Model
by Parasuraman Padmanabhan, Jia Lu, Kian Chye Ng, Dinesh Kumar Srinivasan, Kumar Sundramurthy, Lizanne Greer Nilewski, William K. A. Sikkema, James M. Tour, Thomas A. Kent, Balázs Gulyás and Jan Carlstedt-Duke
Biomedicines 2024, 12(12), 2832; https://doi.org/10.3390/biomedicines12122832 - 13 Dec 2024
Cited by 2 | Viewed by 1075
Abstract
Traumatic brain injury (TBI) causes multiple cerebrovascular disruptions and oxidative stress. These pathological mechanisms are often accompanied by serious impairment of cerebral blood flow autoregulation and neuronal and glial degeneration. Background/Objectives: Multiple biochemical cascades are triggered by brain damage, resulting in reactive oxygen [...] Read more.
Traumatic brain injury (TBI) causes multiple cerebrovascular disruptions and oxidative stress. These pathological mechanisms are often accompanied by serious impairment of cerebral blood flow autoregulation and neuronal and glial degeneration. Background/Objectives: Multiple biochemical cascades are triggered by brain damage, resulting in reactive oxygen species production alongside blood loss and hypoxia. However, most currently available early antioxidant therapies lack capacity and hence sufficient efficacy against TBI. The aim of this study was to test a novel catalytic antioxidant nanoparticle to alleviate the damage occurring in blast TBI. Methods: TBI was elicited in an open blast rat model, in which the rats were exposed to the effects of an explosive blast. Key events of the post-traumatic chain in the brain parenchyma were studied using immunohistochemistry. The application of a newly developed biologically compatible catalytic superoxide dismutase mimetic carbon-based nanocluster, a poly-ethylene-glycol-functionalized hydrophilic carbon cluster (PEG-HCC), was tested post-blast to modulate the components of the TBI process. Results: The PEG-HCC was shown to significantly ameliorate neuronal loss in the brain cortex, the dentate gyrus, and hippocampus when administered shortly after the blast. There was also a significant increase in endothelial activity to repair blood–brain barrier damage as well as the modulation of microglial and astrocyte activity and an increase in inducible NO synthase in the cortex. Conclusions: We have demonstrated qualitatively and quantitatively that the previously demonstrated antioxidant properties of PEG-HCCs have a neuroprotective effect after traumatic brain injury following an explosive blast, acting at multiple levels of the pathological chain of events elicited by TBI. Full article
(This article belongs to the Special Issue Emerging Trends in Traumatic Brain Injury)
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