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Med Hypotheses. 2009 Dec;73(6):994-5. doi: 10.1016/j.mehy.2008.10.041. Epub 2009 Jun 27.

Anti-protein aggregation is a potential target for preventing delayed neuronal death after transient ischemia.

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  • 1Department of Neurosurgery, Xuanwu hospital, Capital Univeristy of Medical Science, 45 Changchun Street, Beijing 100053, PR China.

Abstract

Brain ischemia has been an important risk factor for human being health, there is no effective medicine can be used to protect delayed neuronal injury or death secondary to blood reperfusion following ischemia. Recent discovery shows protein aggregation is an important factor resulting in ischemia-induced neuron death. Therefore, we propose the hypothesis that inhibiting protein aggregation may be an effective way to prevent delayed neuronal death after transient ischemia. At present, in vitro studies show some chemicals such as 4PBA (sodium 4-phenylbutyrate) and trehalose have the features of antagonizing protein aggregation in vitro. Moreover, polyQ-binding peptide (QBP1), geldanamycin, amino acids and amino acid derivatives have been also used in vitro to decrease aggregation and to increase protein stability. Although in vivo and systematical study should be performed to evaluate their effects of anti-protein aggregation, this enlightening us on using them to protect ischemic-induced neuronal death, and find new potential chemicals or methods which could be effective in keeping protein stable and prevent forming aggregates.

PMID:
19560879
[PubMed - indexed for MEDLINE]
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