Traumatic Brain Injury is considered one of the most prevalent causes of death around the world; more than seventy millions of individuals sustain the condition per year. The consequences of traumatic brain injury on brain tissue are complex and multifactorial, hence, the current palliative treatments are limited to improve patients' quality of life. The subsequent hemorrhage caused by trauma and the ongoing oxidative process generated by biochemical disturbances in the in the brain tissue may increase iron levels and reactive oxygen species. The relationship between oxidative damage and the traumatic brain injury is well known, for that reason, diminishing factors that potentiate the production of reactive oxygen species have a promissory therapeutic use. Iron chelators are molecules capable of scavenging the oxidative damage from the brain tissue and are currently in use for ironoverload- derived diseases. Here, we show an updated overview of the underlying mechanisms of the oxidative damage after traumatic brain injury. Later, we introduced the potential use of iron chelators as neuroprotective compounds for traumatic brain injury, highlighting the action mechanisms of iron chelators and their current clinical applications.
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http://dx.doi.org/10.2174/1381612825666191111153802 | DOI Listing |
J Neurotrauma
January 2025
Department of Neurosurgery, the First Medical Centre, Chinese PLA General Hospital, Beijing, China.
Following traumatic brain injury (TBI), inhibition of the Na-K-Cl cotransporter1 (NKCC1) has been observed to alleviate damage to the blood-brain barrier (BBB). However, the underlying mechanism for this effect remains unclear. This study aimed to investigate the mechanisms by which inhibiting the NKCC1 attenuates disruption of BBB integrity in TBI.
View Article and Find Full Text PDFEur Neuropsychopharmacol
January 2025
National PTSD Research Centre at the Thompson Institute, University of the Sunshine Coast, Birtinya, QLD, 4575, Australia. Electronic address:
Mol Neurobiol
January 2025
Department of Pathology, Faculty of Veterinary Medicine, Burdur Mehmet Akif Ersoy University, Burdur, Turkey.
Secondary brain damageafter traumatic brain injury (TBI) involves oxidative stress, neuroinflammation, apoptosis, and necroptosis and can be reversed by understanding these molecular pathways. The objective of this study was to examine the impact of tasimelteon (Tasi) administration on brain injury through the nuclear factor erythroid 2-related factor 2 (NRF-2)/heme oxygenase-1 (HO-1) and receptor-interacting protein kinase 1 (RIPK1)/receptor-interacting protein kinase 3 (RIPK3)/mixed lineage kinase domain-like (MLKL) pathways in rats with TBI. Thirty-two male Wistar albino rats weighing 300-350 g were randomly divided into four groups: the control group, trauma group, Tasi-1 group (trauma + 1 mg/kg Tasi intraperitoneally), and Tasi-10 group (trauma + 10 mg/kg Tasi intraperitoneally).
View Article and Find Full Text PDFCrit Care Med
January 2025
Department of Surgery, Neurology and Neurosurgery Unit, Federal University of Góias, Góias, Brazil.
Objectives: Balancing oxygen requirements, neurologic outcomes, and systemic complications from transfusions in traumatic brain injury (TBI) patients is challenging. This review compares liberal and restrictive transfusion strategies in TBI patients.
Data Sources: Electronic databases were searched from inception to October 2024.
Disabil Rehabil
January 2025
Centre for Aging SMART at Vancouver Coastal Health, Vancouver, BC, Canada.
Purpose: Mental health conditions after mild traumatic brain injury (mTBI) are common and can complicate injury outcomes, but are under-treated. According to the Common Sense Model of Self-Regulation, the way patients perceive their health conditions can influence the way they manage them, including if, when, and how they seek treatment. This study explored how individuals perceive persistent symptoms after mTBI, in order to develop a grounded theory about what motivates and demotivates them to seek mental health treatment after their injury.
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