Mini Review ARTICLE
Genetic factors and manganese-induced neurotoxicity
- Department of Molecular Pharmacology, Albert Einstein College of Medicine, Bronx, NY, USA
Manganese (Mn), is a trace metal required for normal physiological processes in humans. Mn levels are tightly regulated, as high levels of Mn result in accumulation in the brain and cause a neurological disease known as manganism. Manganism shares many similarities with Parkinson’s disease (PD), both at the physiological level and the cellular level. Exposure to high Mn-containing environments increases the risk of developing manganism. Mn is absorbed primarily through the intestine and then released in the blood. Excessive Mn is secreted in the bile and excreted in feces. Mn enters and exits cells through a number of non-specific importers localized on the cell membrane. Mutations in one of the Mn exporters, SLC30A10 (solute carrier family 30, member 10), result in Mn induced toxicity with liver impairments and neurological dysfunction. Four PD genes have been identified in connection to regulation of Mn toxicity, shedding new light on potential links between manganism and PD.
Keywords: manganese, manganism, Parkinson’s disease, neurotoxicity
Citation: Chen P, Parmalee N and Aschner M (2014) Genetic Factors and Manganese-Induced Neurotoxicity. Front. Genet. 5:265. doi: 10.3389/fgene.2014.00265
Received: 21 April 2014; Accepted: 18 July 2014;
Published online: 04 August 2014.
Edited by:Nora L. Nock, Case Western Reserve University, USA
Reviewed by:Marsha Ann Wilcox, Janssen Pharmaceutical Research and Development, USA
Martin Kolisek, Freie Universität Berlin, Germany
Krishnan Sriram, Centers for Disease Control – National Institute for Occupational Safety and Health, USA
Copyright © 2014 Chen, Parmalee and Aschner. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
*Correspondence: Michael Aschner, Department of Molecular Pharmacology, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, USA e-mail: email@example.com