Background: The aim of this study was to evaluate the therapeutic efficiency of Anakinra, an IL-1ß antagonist with anti-inflammatory effects, in an experimental model of traumatic brain injury (TBI).
Methods: Fifty-four rats underwent TBI after a weighted object was dropped onto a metal disc secured to their skulls. Animals were randomized into 3 main groups: control (n=18), TBI + saline (n=18; six animals per time-point) with samples obtained at the first, sixth and twenty-fourth h postoperatively, and TBI + Anakinra (n=18; six animals per time-point) with brain samples obtained at the first, sixth and twenty-fourth h postoperatively. Brain tissue and blood serum were extracted for the analysis of IL-1ß, malondialdehyde, glutathione peroxidase, superoxide dismutase, and catalase levels. Tissue sections were evaluated histopathologically under a light microscope.
Results: After trauma, tissue and serum IL-1ß levels were significantly elevated and after Anakinra administration, these levels substantially decreased. Glutathione peroxidase, superoxide dismutase, and catalase activity decreased following TBI and Anakinra administration proved effective in increasing the activity of these antioxidant enzymes. Histopathological analysis confirmed that Anakinra might protect the brain tissue and nerve cells from injury.
Conclusion: Results demonstrate that Anakinra reduces the development of inflammation and tissue injury events associated with TBI.
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http://dx.doi.org/10.5505/tjtes.2015.57894 | DOI Listing |
Nat Commun
January 2025
Unit on the Development of Neurodegeneration, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD, USA.
Traumatic brain injury (TBI) is a risk factor for neurodegeneration, however little is known about how this kind of injury alters neuron subtypes. In this study, we follow neuronal populations over time after a single mild TBI (mTBI) to assess long ranging consequences of injury at the level of single, transcriptionally defined neuronal classes. We find that the stress-responsive Activating Transcription Factor 3 (ATF3) defines a population of cortical neurons after mTBI.
View Article and Find Full Text PDFJ Neurosurg Case Lessons
January 2025
The Trauma and Neuroscience Institutes, St. John's Hospital and Medical Center, Tulsa, Oklahoma.
Background: Direct carotid-cavernous fistulas (CCFs) are relatively rare but dangerous complications of penetrating traumatic brain injury or maxillofacial trauma. A variety of clinical signs have been described, including ophthalmological and neurological ones. In some cases, severely altered cerebral blood flow can present as massive life-threatening bleeding through the nose, subarachnoid hemorrhage, and/or intraparenchymal hemorrhage.
View Article and Find Full Text PDFDev Med Child Neurol
January 2025
Department of Rehabilitation, Children's Hospital of Chongqing Medical University, Chongqing, China.
Aim: To explore the trajectories of consciousness recovery and prognosis-associated predictors in children with prolonged disorder of consciousness (pDoC).
Method: This single-centre, retrospective, observational cohort involved 134 (87 males, 47 females) children diagnosed with pDoC and hospitalized at the Department of Rehabilitation at the Children's Hospital of Chongqing Medical University in China. The median onset age was 30 (interquartile range [IQR] 18-54) months, with onset ages ranging from 3 to 164 months.
Mil Med
January 2025
Primary Care Department, Touro College of Osteopathic Medicine-Middletown Campus, Middletown, NY 10940, USA.
Concussions are a common form of mild traumatic brain injury characterized by a transient alteration of cerebral function leading to a range of physical, cognitive, and emotional symptoms. Postconcussive symptoms (PCSs) usually resolve in about a week but can persist in 10% to 15% of patients. If left untreated, PCS can profoundly affect a patient's life.
View Article and Find Full Text PDFImmun Inflamm Dis
January 2025
Department of Medical Biochemistry, Institute of Health, Dambi Dollo University, Dambi Dolo, Ethiopia.
Background: The pathomechanism of blast traumatic brain injury (TBI) and blunt TBI is different. In blast injury, evidence indicates that a single blast exposure can often manifest long-term neurological impairments. However, its pathomechanism is still elusive, and treatments have been symptomatic.
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