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锰诱导的帕金森病:来自流行病学和实验研究的证据。

Manganese-Induced Parkinsonism: Evidence from Epidemiological and Experimental Studies.

机构信息

Department of Environmental Health Sciences, Florida International University, Miami, FL 33199, USA.

Biomolecular Sciences Institute, Florida International University, Miami, FL 33199, USA.

出版信息

Biomolecules. 2023 Jul 30;13(8):1190. doi: 10.3390/biom13081190.

DOI:10.3390/biom13081190
PMID:37627255
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10452806/
Abstract

Manganese (Mn) exposure has evolved from acute, high-level exposure causing manganism to low, chronic lifetime exposure. In this latter scenario, the target areas extend beyond the globus pallidus (as seen with manganism) to the entire basal ganglia, including the substantia nigra pars compacta. This change of exposure paradigm has prompted numerous epidemiological investigations of the occurrence of Parkinson's disease (PD), or parkinsonism, due to the long-term impact of Mn. In parallel, experimental research has focused on the underlying pathogenic mechanisms of Mn and its interactions with genetic susceptibility. In this review, we provide evidence from both types of studies, with the aim to link the epidemiological data with the potential mechanistic interpretation.

摘要

锰(Mn)暴露已经从急性、高水平暴露导致的锰中毒演变为低水平、慢性终生暴露。在后一种情况下,靶区不仅包括苍白球(如锰中毒所见),还包括整个基底节,包括黑质致密部。这种暴露模式的变化促使人们对由于 Mn 的长期影响而导致的帕金森病(PD)或帕金森综合征的发生进行了大量的流行病学研究。与此同时,实验研究也集中在 Mn 的潜在发病机制及其与遗传易感性的相互作用上。在这篇综述中,我们提供了这两种类型研究的证据,旨在将流行病学数据与潜在的机制解释联系起来。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad5a/10452806/637988a8cb62/biomolecules-13-01190-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad5a/10452806/637988a8cb62/biomolecules-13-01190-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad5a/10452806/637988a8cb62/biomolecules-13-01190-g001.jpg

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