锰在阿尔茨海默病和帕金森病中的作用的新见解。
New Insights on the Role of Manganese in Alzheimer's Disease and Parkinson's Disease.
机构信息
Department of Molecular Pharmacology, Albert Einstein College of Medicine, Bronx, NY 10461, USA.
Department of Human Anatomy, School of Health and Health Technology, Federal University of Technology Akure, Akure 340252, Nigeria.
出版信息
Int J Environ Res Public Health. 2019 Sep 22;16(19):3546. doi: 10.3390/ijerph16193546.
Abstract
Manganese (Mn) is an essential trace element that is naturally found in the environment and is necessary as a cofactor for many enzymes and is important in several physiological processes that support development, growth, and neuronal function. However, overexposure to Mn may induce neurotoxicity and may contribute to the development of Alzheimer's disease (AD) and Parkinson's disease (PD). The present review aims to provide new insights into the involvement of Mn in the etiology of AD and PD. Here, we discuss the critical role of Mn in the etiology of these disorders and provide a summary of the proposed mechanisms underlying Mn-induced neurodegeneration. In addition, we review some new therapy options for AD and PD related to Mn overload.
摘要
锰（Mn）是一种必需的微量元素，自然存在于环境中，是许多酶的辅助因子，对支持发育、生长和神经元功能的几个生理过程很重要。然而，锰暴露过量可能会引起神经毒性，并可能导致阿尔茨海默病（AD）和帕金森病（PD）的发展。本综述旨在提供对 Mn 参与 AD 和 PD 发病机制的新见解。在这里，我们讨论了 Mn 在这些疾病发病机制中的关键作用，并总结了 Mn 诱导神经退行性变的潜在机制。此外，我们还回顾了一些与 Mn 过载相关的 AD 和 PD 的新治疗选择。
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Manganese promotes the aggregation and prion-like cell-to-cell exosomal transmission of α-synuclein.锰促进α-突触核蛋白的聚集和朊病毒样细胞外泌体传递。
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Mn-Induced Neurocytes Injury and Autophagy Dysfunction in Alpha-Synuclein Wild-Type and Knock-Out Mice: Highlighting the Role of Alpha-Synuclein.锰诱导的神经细胞损伤和自噬功能障碍在α-突触核蛋白野生型和敲除小鼠中的作用：强调α-突触核蛋白的作用。
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