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MeSH Review

Nerve Degeneration

 
 
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Disease relevance of Nerve Degeneration

 

Psychiatry related information on Nerve Degeneration

 

High impact information on Nerve Degeneration

 

Chemical compound and disease context of Nerve Degeneration

  • In the present study, we tested the hypothesis that 17beta-estradiol (betaE2) is a neuroprotectant in the retina, using two experimental approaches: 1) hydrogen peroxide (H(2)O(2))-induced retinal neuron degeneration in vitro, and 2) light-induced photoreceptor degeneration in vivo [13].
  • We demonstrated that both betaE2 and 17alpha-estradiol (alphaE2) significantly protected against H(2)O(2)-induced retinal neuron degeneration; however, progesterone had no effect. betaE2 transiently increased the phosphoinositide 3-kinase (PI3K) activity, when phosphoinositide 4,5-bisphosphate and [(32)gammaATP] were used as substrate [13].
  • Because 6-hydroxydopamine (6-OHDA) is thought to induce nigrostriatal dopaminergic neuronal lesions via metal-catalyzed free radical formation, the effect of the iron chelator desferrioxamine was investigated on 6-OHDA-induced dopaminergic neuron degeneration in the rat [14].
  • During the interval of nerve degeneration, there was a significant reduction of bromodeoxyuridine incorporation from 24 h of nerve injury (39 +/- 7% of the control side, p 0.01) [15].
  • Reductions in muscimol binding to the gamma-aminobutyric acidA receptor had the closest relationship with neuron degeneration, whereas pirenzepine binding appeared to reflect a compensation in muscarinic receptors for changes in neuron densities [16].
 

Biological context of Nerve Degeneration

 

Anatomical context of Nerve Degeneration

 

Gene context of Nerve Degeneration

 

Analytical, diagnostic and therapeutic context of Nerve Degeneration

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