...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>The European Journal of Neuroscience >Brain dopamine neurone 'damage': methamphetamine users vs. Parkinson's disease - a critical assessment of the evidence
【24h】

Brain dopamine neurone 'damage': methamphetamine users vs. Parkinson's disease - a critical assessment of the evidence

机译：脑多巴胺神经元“损伤”：甲基苯丙胺用户与帕金森病 - 对证据的关键评估

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

The objective of this review is to evaluate the evidence that recreational methamphetamine exposure might damage dopamine neurones in human brain, as predicted by experimental animal findings. Brain dopamine marker data in methamphetamine users can now be compared with those in Parkinson's disease, for which the Oleh Hornykiewicz discovery in Vienna of a brain dopamine deficiency is established. Whereas all examined striatal (caudate and putamen) dopamine neuronal markers are decreased in Parkinson's disease, levels of only some (dopamine, dopamine transporter) but not others (dopamine metabolites, synthetic enzymes, vesicular monoamine transporter 2) are below normal in methamphetamine users. This suggests that loss of dopamine neurones might not be characteristic of methamphetamine exposure in at least some human drug users. In methamphetamine users, dopamine loss was more marked in caudate than in putamen, whereas in Parkinson's disease, the putamen is distinctly more affected. Substantia nigra loss of dopamine-containing cell bodies is characteristic of Parkinson's disease, but similar neuropathological studies have yet to be conducted in methamphetamine users. Similarly, it is uncertain whether brain gliosis, a common feature of brain damage, occurs after methamphetamine exposure in humans. Preliminary epidemiological findings suggest that methamphetamine use might increase risk of subsequent development of Parkinson's disease. We conclude that the available literature is insufficient to indicate that recreational methamphetamine exposure likely causes loss of dopamine neurones in humans but does suggest presence of a striatal dopamine deficiency that, in principle, could be corrected by dopamine substitution medication if safety and subject selection considerations can be resolved.
机译：本综述的目的是评估娱乐甲基苯丙胺暴露可能会损害人脑中多巴胺神经元的证据，如通过实验动物发现所预测的。脑多胺标志物数据现在可以与帕金森病的甲基苯丙胺用户中的数据进行比较，为此建立了大脑多巴胺缺乏的维也纳的Oleh Hornykiewicz发现。虽然所有检查的纹状体（尾状和腐烂）多巴胺神经元标志物在帕金森病中减少，但只有一些（多巴胺，多巴胺转运蛋白）但不是其他（多巴胺代谢物，合成酶，尿囊单胺转运蛋白转运蛋白转运蛋白转运蛋白转运蛋白转运物2）。这表明失去多巴胺神经元的失去可能在至少一些人吸毒者中的甲基苯丙胺暴露的特征。在甲基苯丙胺使用者中，多巴胺损失在凯伦比凯伦更加标记，而在帕金森病中，腐败明显受到影响。 Imageia NIGRA失去多巴胺的细胞体的丧失是帕金森病的特征，但尚未在甲基苯丙胺用户中进行类似的神经病理学研究。同样，在人类的甲基苯丙胺暴露后，脑脊髓症是否是脑渗透率的常见特征不确定。初步流行病学研究结果表明，甲基苯丙胺使用可能会增加随后帕金森病的风险。我们得出结论，可用文献不足以表明娱乐甲基苯丙胺暴露可能导致人类多巴胺神经元失去，但确实提示存在偏纹的多巴胺缺乏，原则上可以通过多巴胺替代药物纠正，如果安全和主题选择考虑因素可以通过多巴胺替代药物纠正得到解决。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号