The neurotoxicity of iron, copper and manganese in Parkinson's and Wilson's diseases
Language English Country Germany Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't, Review
PubMed
24954801
DOI
10.1016/j.jtemb.2014.05.007
PII: S0946-672X(14)00073-X
Knihovny.cz E-resources
- Keywords
- Chelating agents, Copper, Iron, Manganese, Parkinson's disease, Wilson's disease,
- MeSH
- Hepatolenticular Degeneration metabolism physiopathology MeSH
- Homeostasis MeSH
- Humans MeSH
- Manganese metabolism toxicity MeSH
- Copper metabolism toxicity MeSH
- Disease Models, Animal MeSH
- Brain metabolism physiopathology MeSH
- Parkinson Disease metabolism physiopathology MeSH
- Environmental Exposure adverse effects MeSH
- Iron metabolism toxicity MeSH
- Animals MeSH
- Check Tag
- Humans MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Review MeSH
- Names of Substances
- Manganese MeSH
- Copper MeSH
- Iron MeSH
Impaired cellular homeostasis of metals, particularly of Cu, Fe and Mn may trigger neurodegeneration through various mechanisms, notably induction of oxidative stress, promotion of α-synuclein aggregation and fibril formation, activation of microglial cells leading to inflammation and impaired production of metalloproteins. In this article we review available studies concerning Fe, Cu and Mn in Parkinson's disease and Wilson's disease. In Parkinson's disease local dysregulation of iron metabolism in the substantia nigra (SN) seems to be related to neurodegeneration with an increase in SN iron concentration, accompanied by decreased SN Cu and ceruloplasmin concentrations and increased free Cu concentrations and decreased ferroxidase activity in the cerebrospinal fluid. Available data in Wilson's disease suggest that substantial increases in CNS Cu concentrations persist for a long time during chelating treatment and that local accumulation of Fe in certain brain nuclei may occur during the course of the disease. Consequences for chelating treatment strategies are discussed.
2nd Department of Neurology Institute of Psychiatry and Neurology Warsaw Poland
Department of Chemistry Norwegian University of Science and Technology Trondheim Norway
Department of Medicine Innlandet Hospital Trust Kongsvinger Hospital Division Kongsvinger Norway
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