Mievis Stéphane, Levivier Marc, Vassart Gilbert, Brotchi Jacques, Ledent Catherine, Blum David
IRIBHM, University of Brussels, ULB-Erasme, Brussels, Belgium.
Neurobiol Aging. 2007 Dec;28(12):1944-6. doi: 10.1016/j.neurobiolaging.2006.09.011. Epub 2006 Oct 24.
We have evaluated the neuroprotective effects of citicoline in relevant phenotypic models of Huntington's disease induced by either the mitochondrial inhibitor 3-nitropropionic acid or the N-methyl-D-aspartate agonist quinolinic acid, which, respectively, reproduce the metabolic defect or the excitotoxicity seen in the disease. We found that citicoline failed to reverse behavioural and histological alterations induced by both neurotoxins. In addition, citicoline did not reduce PC12 cell death induced by the expression of an N-terminal fragment of mutated Huntingtin. Altogether, our results suggest that citicoline is not a potential therapeutic agent for the treatment of Huntington's disease.
我们已经评估了胞磷胆碱在线粒体抑制剂3-硝基丙酸或N-甲基-D-天冬氨酸激动剂喹啉酸诱导的亨廷顿舞蹈病相关表型模型中的神经保护作用，这两种物质分别再现了该疾病中出现的代谢缺陷或兴奋性毒性。我们发现胞磷胆碱未能逆转这两种神经毒素诱导的行为和组织学改变。此外，胞磷胆碱并未减少由突变型亨廷顿蛋白N端片段表达所诱导的PC12细胞死亡。总之，我们的结果表明胞磷胆碱不是治疗亨廷顿舞蹈病的潜在治疗药物。
