Neuroprotection afforded by prior citicoline administration in experimental brain ischemia: effects on glutamate transport

@article{Hurtado2005NeuroprotectionAB,
  title={Neuroprotection afforded by prior citicoline administration in experimental brain ischemia: effects on glutamate transport},
  author={Olivia Hurtado and Mar{\'i}a Angeles Moro and Antonio C{\'a}rdenas and Ver{\'o}nica S{\'a}nchez and Paz Fern{\'a}ndez-Tom{\'e} and Juan Carlos Leza and Pedro Lorenzo and Julio J Secades and Rafael Lozano and Antoni D{\'a}valos and Jos{\'e} Castillo and Ignacio Lizasoain},
  journal={Neurobiology of Disease},
  year={2005},
  volume={18},
  pages={336-345}
}
BACKGROUND AND PURPOSE Cytidine-5'-diphosphocholine (citicoline or CDP-choline), an intermediate in the biosynthesis of phosphatidylcholine, has shown beneficial effects in a number of CNS injury models including cerebral ischemia. Citicoline is the only neuroprotectant that has proved efficacy in patients with moderate to severe stroke. However, the precise mechanism by which citicoline is neuroprotective is not fully known. The present study was designed to search for mechanisms of citicoline… Expand
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References

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TLDR
The data indicated that the effects of citicoline on phospholipids occurred primarily during the first day of reperfusions, with effects on glutathione being important over the 3-day reperfusion period. Expand
Citicoline: neuroprotective mechanisms 
in cerebral ischemia
TLDR
The studies in transient cerebral ischemia suggest that citicoline might enhance reconstruction of PtdCho and sphingomyelin, but could act by inhibiting the destructive processes (activation of phospholipases), and a singular unifying unifying mechanism has been hypothesized. Expand
The effects of prolonged treatment with citicoline in temporary experimental focal ischemia
TLDR
It is demonstrated that extended high dose citicoline treatment significantly reduced infarct volume in this temporary focal ischemia model and that there was a trend toward reducing brain edema and mortality. Expand
Citicoline decreases phospholipase A2 stimulation and hydroxyl radical generation in transient cerebral ischemia
TLDR
It is suggested that citicoline affects PLA2 stimulation and decreases OH· generation after transient cerebral ischemia, which is major factors causing neuronal injury in CNS trauma and neurodegenerative diseases. Expand
Citicoline protects hippocampal neurons against apoptosis induced by brain beta-amyloid deposits plus cerebral hypoperfusion in rats.
TLDR
It was concluded that citicoline exerts antiapoptotic, neuroprotective and antiamnesic effects in conditions of neurodegeneration induced by A beta 4 plus hypoperfusion. Expand
Citicoline mechanisms and clinical efficacy in cerebral ischemia
TLDR
The clinical efficacy of citicoline should be examined further in light of the recent phase III stroke clinical trials and experimental data for cerebral ischemia and several factors that might have hindered efficacy in stroke clinical Trials in the United States are evaluated. Expand
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TLDR
CDP-choline has beneficial effects on brain dysfunction induced by cerebral ischemia, which may be due in part to the restorative effects of CDP- choline on disturbed cerebral glucose metabolism, probably by stimulating phospholipid biosynthesis. Expand
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TLDR
It is concluded that citicoline may offer significant neuronal protection that may be further enhanced with the addition of a thrombolytic agent. Expand
Diazepam Promotes ATP Recovery and Prevents Cytochrome c Release in Hippocampal Slices After In Vitro Ischemia
TLDR
Benzodiazepines protect hippocampal neurons when administered within the first few hours after transient cerebral ischemia, and complete recovery of ATP and prevention of cytochrome c release from mitochondria can be achieved when diazepam is given after the loss of ATP induced by OGD. Expand
Inhibition of glutamate release by delaying ATP fall accounts for neuroprotective effects of antioxidants in experimental stroke
TLDR
Results show that intraperitoneal administration of antioxidants 2 h before MCAO enhances ATP synthesis and causes a neuroprotective effect concomitant to inhibition of ischemia‐induced increase in brain glutamate, and may possess important therapeutic repercussions in the management of ischemic stroke. Expand
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