Neuroprotection targets after traumatic brain injury

@article{Wang2006NeuroprotectionTA,
  title={Neuroprotection targets after traumatic brain injury},
  author={Kevin K. W. Wang and S. F. Larner and Gillian Robinson and R. L. Hayes},
  journal={Current Opinion in Neurology},
  year={2006},
  volume={19},
  pages={514–519}
}
Purpose of reviewThe scarcity of pharmacological neuroprotective treatments for traumatic brain injury is a concern being targeted on various fronts. This review examines the latest treatments under investigation. Recent findingsIn the last 12–18 months, no drug has completed phase III clinical trials as a clearly proven method to treat traumatic brain injury. While the drugs work in rodents, when they make it to clinical trial they have failed primarily due to negative side-effects. Those… 
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  • 2007
TLDR
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TLDR
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TLDR
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Neuroprotection against Traumatic Brain Injury by Xenon, but Not Argon, Is Mediated by Inhibition at the N-Methyl-D-Aspartate Receptor Glycine Site
TLDR
Xenon neuro protection against traumatic brain injury can be reversed by increasing the glycine concentration, consistent with inhibition at the N-methyl-D-aspartate receptor glycine site playing a significant role in xenon neuroprotection.
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TLDR
A critical overview of the literature on CsA neuroprotective effects in animal studies and current findings of clinical trials in the treatment of TBI with an emphasis on the possibleCsA molecular mechanism of action is provided.
The nitrone free radical scavenger NXY-059 is neuroprotective when administered after traumatic brain injury in the rat.
TLDR
Results show that post-injury treatment with NXY-059 significantly attenuated the loss of injured brain tissue and improved cognitive outcome, suggesting a major role for ROS in the pathophysiology of TBI.
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