Molecular neurotoxicological models of Parkinsonism: focus on genetic manipulation of mice
Molecular neurotoxicological models of Parkinsonism: focus on genetic manipulation of mice
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DOI：
10.1016/s1353-8020(01)00021-9
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发表时间：
2001-10-01
影响因子：
4.1
通讯作者：
Cadet, JL
中科院分区：
文献类型：
--
作者：
Cadet, JL
帕金森病是一种主要影响人类黑质纹状体多巴胺能系统的神经退行性疾病。已经提出了几个命题来解释这种综合征的细胞和分子病理生物学。最初的尝试是通过使用各种药物来操纵毒素在体外和体内破坏多巴胺能细胞的有害作用。这些研究表明，氧化应激是杀死这些细胞的一个重要因素。最近的一些尝试是利用转基因小鼠来消除或过度表达感兴趣的基因。这些实验表明，多巴胺能细胞的破坏可能是依赖和独立分子途径趋同的结果，并且触发的细胞事件可能导致这些多巴胺能细胞的死亡。(C) 2001年Elsevier Science Ltd.出版
Parkinson's disease is a neurodegenerative disorder that affects mainly the nigrostriatal doparminergic system in humans. Several propositions have been put forward to explain the cellular and molecular pathobiology of this syndrome. Initial attempts were made through the use of various agents to manipulate the deleterious effects of toxins that destroy dopaminergic cells both in vitro and in vivo. These studies led to the idea that oxidative stress is an important factor in killing these cells. More recent attempts have made use of genetically modified mice to eliminate or over-express genes of interest. These experiments have suggested that the destruction of dopaminergic cells might be the result of the convergence of dependent and independent molecular pathways and that trigger cellular events might lead to the demise of these doparninergic cells. (C) 2001 Published by Elsevier Science Ltd.