Tag: traumatic brain injury

N-acetylcysteine (NAC) in neurological disorders: mechanisms of action and therapeutic opportunities

This 2014 review outlines the therapeutic potential and mechanisms of N-acetylcysteine (NAC) in treating various neurological disorders. As a precursor to glutathione, NAC plays a critical role in reducing oxidative stress and modulating inflammation. It influences glutamatergic neurotransmission, restores redox balance, and promotes neuronal survival. The review highlights preclinical and

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Brain Recovery after a Plane Crash: Treatment with Growth Hormone (GH) and Neurorehabilitation: A Case Report

This case report describes a young male patient who suffered severe traumatic brain injury (TBI) following a plane crash, resulting in spastic tetraplegia, dysarthria, dysphagia, cognitive deficits, and joint deformities. Fifteen months post-injury, the patient commenced a regimen of growth hormone (GH) therapy at 1 mg/day administered in three-month intervals

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Serum Insulin-Like Growth Factor-I Levels Are Associated with Improved White Matter Recovery After Traumatic Brain Injury

This 2017 longitudinal cohort study by Feeney et al. examined whether serum insulin-like growth factor-I (IGF-I) levels influence white matter (WM) recovery and cognitive outcomes in adults with moderate to severe traumatic brain injury (TBI). Using diffusion tensor imaging (DTI) and neuropsychological assessments over a 13-month period, the study found

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Novel Actions of Progesterone: What We Know Today and What Will Be the Scenario in the Future?

This 2012 review highlights emerging non-reproductive roles of progesterone, including potential therapeutic applications in traumatic brain injury (TBI), stroke, Alzheimer’s disease, diabetic neuropathy, and crush injuries. Preclinical and early clinical studies suggest that progesterone and its derivatives, such as norethisterone and megestrol acetate, may offer neuroprotective and anti-inflammatory benefits. Additionally,

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From Mitochondrial Function to Neuroprotection-an Emerging Role for Methylene Blue

This review explores the potential neuroprotective role of methylene blue (MB), particularly its ability to enhance mitochondrial function in neurodegenerative diseases such as Alzheimer’s disease, Parkinson’s disease, stroke, and traumatic brain injury. MB acts as an alternative electron carrier in the mitochondrial electron transport chain, improving ATP production and reducing

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Methylene blue and its potential in the treatment of traumatic brain injury, brain ischemia, and Alzheimer’s disease

This article explores the potential therapeutic applications of methylene blue (MB) in treating neurodegenerative conditions like traumatic brain injury, brain ischemia, and Alzheimer’s disease. MB demonstrates multiple beneficial effects, including anti-apoptotic and anti-inflammatory actions, inhibition of protein aggregation, activation of autophagy, and modulation of mitochondrial function. These properties suggest that

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Methylene blue attenuates traumatic brain injury-associated neuroinflammation and acute depressive-like behavior in mice

This study highlights the neuroprotective effects of methylene blue (MB) in various brain injury models. MB was shown to reduce neuroinflammation and improve neurological function in traumatic brain injury (TBI) and subarachnoid hemorrhage (SAH) models. It achieved these effects through modulation of inflammatory pathways, particularly the Akt/GSK-3β/MEF2D signaling pathway. MB

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Methylene blue exerts a neuroprotective effect against traumatic brain injury by promoting autophagy and inhibiting microglial activation

This study investigates the neuroprotective effects of methylene blue (MB) in a traumatic brain injury (TBI) mouse model. MB administration resulted in a significant reduction in brain water content and neuronal death, indicating its potential to protect the brain after TBI. The study also found that MB promoted autophagy and

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Hyperbaric Oxygen Therapy Alleviates Memory and Motor Impairments Following Traumatic Brain Injury via the Modulation of Mitochondrial-Dysfunction-Induced Neuronal Apoptosis in Rats

This animal study investigated the neuroprotective effects of hyperbaric oxygen therapy (HBOT) in rats with traumatic brain injury (TBI). The results showed that HBOT significantly improved motor and spatial learning performance, reduced cortical neuronal loss, and decreased the apoptosis marker cleaved-Caspase3. Additionally, HBOT preserved mitochondrial respiration functions and modulated glial

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