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Published on: May 4, 2020
Manganese homeostasis and transport
Jerome Roth1, Silvia Ponzoni, Michael Aschner
1Department of Pharmacology and Toxicology, University at Buffalo School of Medicine, 11 Cary Hall, Buffalo, NY, 14214, USA.
Manganese (Mn) accumulation causes neurotoxicity and neurodegeneration, particularly affecting mitochondria and glia. Gene-environment interactions, especially with Parkinson's disease (PD) genes, influence Mn sensitivity.
Area of Science:
- Neuroscience
- Toxicology
- Environmental Health
Background:
- Manganese (Mn) is an essential element, but excessive accumulation can lead to neurotoxicity.
- Neurodegenerative processes are complex and can be influenced by environmental factors.
- Mitochondrial dysfunction and glial cell involvement are implicated in various neurological disorders.
Purpose of the Study:
- To review the mechanisms of manganese accumulation and transport.
- To elucidate the neurotoxic effects and neurodegeneration pathways induced by manganese.
- To explore the role of gene-environment interactions in manganese-induced neurotoxicity, with a focus on Parkinson's disease.
Main Methods:
- Literature review of existing studies on manganese neurotoxicity.
- Analysis of research on manganese transport mechanisms.
- Examination of studies investigating mitochondrial and glial roles in neurodegeneration.
- Review of genetic and environmental interaction studies related to Parkinson's disease and manganese.
Main Results:
- Manganese accumulation is linked to specific transport mechanisms.
- Neurotoxicity involves complex pathways affecting neuronal function.
- Mitochondria and glia play critical roles in manganese-induced neurodegeneration.
- Genetic factors can modify an individual's susceptibility to manganese toxicity.
Conclusions:
- Manganese exposure poses a significant risk for neurodegeneration.
- Understanding manganese transport and cellular mechanisms is crucial for developing interventions.
- Gene-environment interactions are key determinants of individual vulnerability to manganese neurotoxicity, particularly in the context of Parkinson's disease.
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