Related Experiment Video
Updated: Apr 25, 2026

Gene-environment Interaction Models to Unmask Susceptibility Mechanisms in Parkinson's Disease
Published on: January 7, 2014
Genetic factors and manganese-induced neurotoxicity
Pan Chen1, Nancy Parmalee1, Michael Aschner1
1Department of Molecular Pharmacology, Albert Einstein College of Medicine Bronx, NY, USA.
Abstract:
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.
Insights
High manganese (Mn) exposure can cause manganism, a neurological disease similar to Parkinson's disease (PD). Understanding Mn transport and its link to PD genes is crucial for potential treatments.
Area of Science:
- Neuroscience
- Toxicology
- Genetics
Background:
- Manganese (Mn) is an essential trace metal, but excessive levels lead to neurotoxicity and manganism.
- Manganism exhibits significant physiological and cellular similarities to Parkinson's disease (PD).
Purpose of the Study:
- To explore the relationship between manganese toxicity and Parkinson's disease.
- To investigate the role of Mn transport mechanisms and associated genes in neurodegeneration.
Main Methods:
- Review of existing literature on manganese metabolism and neurotoxicity.
- Analysis of genetic links between manganese regulation and Parkinson's disease.
Main Results:
- High manganese exposure is a risk factor for manganism, a condition mimicking PD.
- Mutations in the Mn exporter SLC30A10 cause toxicity, affecting liver and neurological function.
- Four PD-associated genes are implicated in regulating manganese toxicity.
Conclusions:
- Manganese homeostasis is critical for preventing neurological dysfunction.
- The identified links between manganese toxicity and PD genes offer new insights into PD pathogenesis.
- Further research into Mn transport and its role in PD is warranted.
More Related Videos
08:36Functional Neuroimaging Using Ultrasonic Blood-brain Barrier Disruption and Manganese-enhanced MRI
Published on: July 12, 2012
04:48Setup of Capillary Electrophoresis-Inductively Coupled Plasma Mass Spectrometry CE-ICP-MS for Quantification of Iron Redox Species FeII, FeIII
Published on: May 4, 2020
Related Concept Videos
Human Genetics
The complex relationship between genetics and psychology is observable through common biological components such...
Drug Toxicity: Dose-Dependent Reactions
Drug Toxicity: Risk factors
Parkinson Disease ll: Pathophysiology
Drugs Affecting Neurotransmitter Synthesis
Drug toxicity: Idiosyncratic Reactions