Chronic but not acute treatment with caffeine attenuates traumatic brain injury in the mouse cortical impact model

@article{Li2008ChronicBN,
  title={Chronic but not acute treatment with caffeine attenuates traumatic brain injury in the mouse cortical impact model},
  author={W. Li and Shuang-Shuang Dai and Jianhong An and P. Li and X. Chen and Ren-ping Xiong and P. Liu and H. Wang and Y. Zhao and M. Zhu and X. Liu and Pei-Fang Zhu and J.-F. Chen and Y. Zhou},
  journal={Neuroscience},
  year={2008},
  volume={151},
  pages={1198-1207}
}
  • W. Li, S. Dai, Y. Zhou
  • Published 19 February 2008
  • Biology, Medicine, Psychology
  • Neuroscience
View on Elsevier
doi.org
90 Citations
Highly Influential Citations
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25
Methods Citations
5
Results Citations
1

90 Citations

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Citation Type

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Chronic caffeine consumption at low doses exerts anti-inflammatory effects and prevents MDMA-induced neuroinflammation.
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Caffeine prevents acute mortality after TBI in rats without increased morbidity
Adenosine A3 receptor as a novel therapeutic target to reduce secondary events and improve neurocognitive functions following traumatic brain injury
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The results provide support for the beneficial effects of small molecule A 3 AR agonists to mitigate secondary tissue injury and cognitive impairment following TBI.
Genetic inactivation of adenosine A2A receptors attenuates acute traumatic brain injury in the mouse cortical impact model
Effects of Preinjury and Postinjury Exposure to Caffeine in a Rat Model of Traumatic Brain Injury.
TLDR
Preexposure of the injured brain to caffeine does not have a major impact on acute and delayed outcome parameters; more importantly, a single acute dose of caffeine after the injury can prevent lethal apnea regardless of chronic caffeine preexposure.
Time-Dependent Bidirectional Neuroprotection by Adenosine 2A Receptor in Experimental Traumatic Brain Injury.
Chronic caffeine exposure attenuates blast-induced memory deficit in mice.
Chronic or high dose acute caffeine treatment protects mice against oleic acid-induced acute lung injury via an adenosine A2A receptor-independent mechanism.
The Many Roles of Adenosine in Traumatic Brain Injury
TLDR
This work reports increases in brain interstitial adenosine levels in patients with severe TBI during episodes of ischemia, and suggests that the newly discovered 2,3-cyclic AMP pathway represents an important component of the adenosines response to TBI.
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The Sodium Channel Blocker and Glutamate Release Inhibitor BW1003C87 and Magnesium Attenuate Regional Cerebral Edema Following Experimental Brain Injury in the Rat
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It is suggested that excitatory neurotransmission may play an important role in the pathogenesis of posttraumatic brain edema and that pre‐ or post‐synaptic blockade of glutamate receptor systems may attenuate part of the deleterious sequelae of traumatic brain injury.
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TLDR
Low dose caffeine exposure (plasma levels corresponding to umbilical cord plasma in newborns of coffee-consuming mothers) reduced HI brain damage by 30% in 7-d-old rats, and this ameliorating effect could not be accounted for by up-regulation of adenosine receptors.
Increases in Cerebrospinal Fluid Caffeine Concentration are Associated with Favorable Outcome after Severe Traumatic Brain injury in Humans
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  • Medicine, Biology
    Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism
  • 2008
TLDR
Caffeine and its metabolites are commonly detected in CSF in patients with severe TBI and in an exploratory assessment are associated with favorable outcome, and it is speculated that caffeine may be neuroprotective by long-term upregulation of adenosine A1 receptors or acute inhibition of A2a receptors.
Caffeine prevents protection in two human models of ischemic preconditioning.
Caffeine protects Alzheimer’s mice against cognitive impairment and reduces brain β-amyloid production
Caffeine's neuroprotection against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine toxicity shows no tolerance to chronic caffeine administration in mice
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Neuroprotection by Caffeine and A2A Adenosine Receptor Inactivation in a Model of Parkinson's Disease
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A potential neural basis for the inverse association of caffeine with the development of PD is established and the potential of A(2A) antagonists as a novel treatment for this neurodegenerative disease is enhanced.
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