Guilarte Tomás R
Neurotoxicology and Molecular Imaging Laboratory, Department of Environmental Health Sciences, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland, USA.
Cien Saude Colet. 2011 Nov;16(11):4549-66. doi: 10.1590/s1413-81232011001200028.
The goal of this review was to examine whether chronic Mn exposure produces dopamine neuron degeneration and PD or whether it has a distinct neuropathology and clinical presentation. I reviewed available clinical, neuroimaging, and neuropathological studies in humans and nonhuman primates exposed to Mn or other human conditions that result in elevated brain Mn concentrations. Human and nonhuman primate literature was examined to compare clinical, neuroimaging, and neuropathological changes associated with Mn-induced parkinsonism. Clinical, neuroimaging, and neuropathological evidence was used to examine whether Mn-induced parkinsonism involves degeneration of the nigrostriatal dopaminergic system as is the case in PD. The overwhelming evidence shows that Mn-induced parkinsonism does not involve degeneration of midbrain dopamine neurons and that l-dopa is not an effective therapy. New evidence is presented on a putative mechanism by which Mn may produce movement abnormalities. Confirmation of this hypothesis in humans is essential to make rational decisions about treatment, devise effective therapeutic strategies, and set regulatory guidelines.
本综述的目的是研究长期锰暴露是否会导致多巴胺能神经元变性和帕金森病（PD），或者它是否具有独特的神经病理学和临床表现。我回顾了关于暴露于锰或其他导致脑锰浓度升高的人类状况的人类和非人类灵长类动物的现有临床、神经影像学和神经病理学研究。研究人类和非人类灵长类动物的文献，以比较与锰诱导的帕金森综合征相关的临床、神经影像学和神经病理学变化。利用临床、神经影像学和神经病理学证据来研究锰诱导的帕金森综合征是否像帕金森病那样涉及黑质纹状体多巴胺能系统的变性。压倒性的证据表明，锰诱导的帕金森综合征不涉及中脑多巴胺能神经元的变性，左旋多巴也不是一种有效的治疗方法。提出了关于锰可能产生运动异常的一种假定机制的新证据。在人类中证实这一假设对于做出合理的治疗决策、制定有效的治疗策略和制定监管指南至关重要。
