Manganese and its role in Parkinson's disease: from transport to neuropathology.
Manganese and its role in Parkinson's disease: from transport to neuropathology.
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DOI：
10.1007/s12017-009-8083-0
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发表时间：
2009
影响因子：
3.5
通讯作者：
Tjalkens R
中科院分区：
文献类型：
--
作者：
Aschner M;Erikson KM;Herrero Hernández E;Tjalkens R
这篇综述的目的是强调与锰暴露相关的神经病理学的最新进展。我们开始讨论职业性锰中毒和临床方面的障碍。其次是新的考虑锰运输（也见章由Yokel，本卷），推进新的假设参与的几个运输锰进入大脑。随后简要描述了Mn对神经递质系统的影响，这些神经递质系统是多巴胺（DA）生物学（Mn神经毒性的主要靶点）的假定调节剂，以及Mn对线粒体功能障碍和细胞能量代谢中断的影响。接下来，我们讨论神经元损伤中神经胶质的炎症激活以及突触传递和神经胶质-神经元通信的中断如何可能作为与神经胶质和神经元之间的串扰相称的Mn诱导的神经变性的潜在机制。最后，我们讨论锰暴露的治疗方面。重点是针对治疗方式和螯合剂的效用，在减轻神经退行性后遗症暴露于锰。关于本综述固有的几个主题以及其他主题的其他阅读，读者可能希望咨询Aschner和Dorman（毒理学综述25：147-154，2007）和。
The purpose of this review is to highlight recent advances in the neuropathology associated with Mn exposures. We commence with a discussion on occupational manganism and clinical aspects of the disorder. This is followed by novel considerations on Mn transport (see also chapter by Yokel, this volume), advancing new hypotheses on the involvement of several transporters in Mn entry into the brain. This is followed by a brief description of the effects of Mn on neurotransmitter systems that are putative modulators of dopamine (DA) biology (the primary target of Mn neurotoxicity), as well as its effects on mitochondrial dysfunction and disruption of cellular energy metabolism. Next, we discuss inflammatory activation of glia in neuronal injury and how disruption of synaptic transmission and glial-neuronal communication may serve as underlying mechanisms of Mn-induced neurodegeneration commensurate with the cross-talk between glia and neurons. We conclude with a discussion on therapeutic aspects of Mn exposure. Emphasis is directed at treatment modalities and the utility of chelators in attenuating the neurodegenerative sequelae of exposure to Mn. For additional reading on several topics inherent to this review as well as others, the reader may wish to consult Aschner and Dorman (Toxicological Review 25:147–154, 2007) and.