| Literature DB >> 31571097 |
Tao Ke1, Marta Sidoryk-Wegrzynowicz2, Edward Pajarillo3, Asha Rizor3, Félix Alexandre Antunes Soares1,4, Eunsook Lee3, Michael Aschner5,6.
Abstract
Manganese (Mn) overexposure is a public health concern due to its widespread industrial usage and the risk for environmental contamination. The clinical symptoms of Mn neurotoxicity, or manganism, share several pathological features of Parkinson's disease (PD). Biologically, Mn is an essential trace element, and Mn in the brain is preferentially localized in astrocytes. This review summarizes the role of astrocytes in Mn-induced neurotoxicity, specifically on the role of neurotransmitter recycling, neuroinflammation, and genetics. Mn overexposure can dysregulate astrocytic cycling of glutamine (Gln) and glutamate (Glu), which is the basis for Mn-induced excitotoxic neuronal injury. In addition, reactive astrocytes are important mediators of Mn-induced neuronal damage by potentiating neuroinflammation. Genetic studies, including those with Caenorhabditis elegans (C. elegans) have uncovered several genes associated with Mn neurotoxicity. Though we have yet to fully understand the role of astrocytes in the pathologic changes characteristic of manganism, significant strides have been made over the last two decades in deciphering the role of astrocytes in Mn-induced neurotoxicity and neurodegeneration.Entities:
Keywords: Astrocyte; Glutamate; Glutamine; Manganese; Neurotoxicity
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Year: 2019 PMID： 31571097 DOI： 10.1007/s11064-019-02881-7
Source DB: PubMed Journal: Neurochem Res ISSN： 0364-3190 Impact factor: 3.996