Traumatic brain injury (TBI) elicits a complex secondary injury response, with neuroinflammation as a crucial central component. Long thought to be solely a deleterious factor, the neuroinflammatory response has recently been shown to be far more intricate, with both beneficial and detrimental consequences depending on the timing, magnitude and specific immune composition of the response post-injury. Despite extensive preclinical and clinical research into mechanisms of secondary injury after TBI, no effective neuroprotective therapy has been identified, with potential candidates repeatedly proving disappointing in the clinic. The neuroinflammatory response offers a promising avenue for therapeutic targeting, aiming to quell the deleterious consequences without influencing its function in providing a neurotrophic environment supportive of repair. The present review firstly describes the findings of recent clinical trials that aimed to modulate inflammation as a means of neuroprotection. Secondly, we discuss promising multifunctional and single-target anti-inflammatory candidates either currently in trial, or with ample experimental evidence supporting clinical application. This article is part of a Special Issue entitled SI:Brain injury and recovery.
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http://dx.doi.org/10.1016/j.brainres.2015.12.024 | DOI Listing |
Cells
December 2024
Institute of Anaesthesiologic Pathophysiology and Process Development, University Hospital Ulm, Helmholtzstrasse 8/1, 89081 Ulm, Germany.
Traumatic brain injury (TBI) remains one of the leading causes of death. Because of the individual nature of the trauma (brain, circumstances and forces), humans experience individual TBIs. This makes it difficult to generalise therapies.
View Article and Find Full Text PDFAnn Neurol
January 2025
Department of Neurology, University of Massachusetts Chan Medical School, Worcester, MA.
Objective: Approximately 20% of familial cases of amyotrophic lateral sclerosis (ALS) are caused by mutations in the gene encoding superoxide dismutase 1 (SOD1). Epidemiological data have identified traumatic brain injury (TBI) as an exogenous risk factor for ALS; however, the mechanisms by which TBI may worsen SOD1 ALS remain largely undefined.
Methods: We sought to determine whether repetitive TBI (rTBI) accelerates disease onset and progression in the transgenic SOD1 mouse ALS model, and whether loss of the primary regulator of axonal degeneration sterile alpha and TIR motif containing 1 (Sarm1) mitigates the histological and behavioral pathophysiology.
Vet Q
December 2025
Department of Physiology, Temerty Faculty of Medicine, University of Toronto, Toronto, Canada.
This review examines the role of the canine blood-brain barrier (BBB) in health and disease, focusing on the impact of the multidrug resistance (MDR) transporter P-glycoprotein (P-gp) encoded by the gene. The BBB is critical in maintaining central nervous system homeostasis and brain protection against xenobiotics and environmental drugs that may be circulating in the blood stream. We revise key anatomical, histological and functional aspects of the canine BBB and examine the role of the gene mutation in specific dog breeds that exhibit reduced P-gp activity and disrupted drug brain pharmacokinetics.
View Article and Find Full Text PDFDisabil Rehabil
January 2025
Department of Women's and Children's Health, Uppsala University, Uppsala, Sweden.
Unlabelled: Children with acquired brain injury (ABI) are at risk of developing cognitive, physical, or emotional impairments that affect their daily lives at home, school, and in society.
Purpose: To explore this, we used the Swedish version of the Child and Family Follow-up Survey (CFFS-SWE) to describe the participation of 39 children (aged 5-17 years) who had sustained ABIs.
Materials And Methods: We assessed their participation using the CFFS-SWE at three points: upon discharge from the acute hospital, six months post-discharge, and between one and four years after discharge.
CNS Neurosci Ther
January 2025
The Key Laboratory of Biomedical Information Engineering of Ministry of Education, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an, China.
Traumatic brain injury (TBI) is one of the most traumatizing and poses serious health risks to people's bodies due to its unique pathophysiological characteristics. The investigations on the pathological mechanism and valid interventions of TBI have attracted widespread attention worldwide. With bio-mimic mechanic cues, the dynamic hydrogels with dynamic stiffness changes or reversible crosslinking have been suggested to construct the in vitro disease models or novel therapeutic agents for TBI.
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