Toxics | |
Abnormal Copper Homeostasis: Mechanisms and Roles in Neurodegeneration | |
关键词: copper; neurotoxicity; ceruloplasmin; cuproenzymes; chaperones; neurodegeneration; brain; Wilson’s disease; Alzheimer’s disease; Parkinson’s disease; | |
DOI : 10.3390/toxics2020327 | |
来源: mdpi | |
【 摘 要 】
As a cofactor of proteins and enzymes involved in critical molecular pathways in mammals and low eukaryotes, copper is a transition metal essential for life. The intra-cellular and extra-cellular metabolism of copper is under tight control, in order to maintain free copper concentrations at very low levels. Copper is a critical element for major neuronal functions, and the central nervous system is a major target of disorders of copper metabolism. Both the accumulation of copper and copper deficiency are associated with brain dysfunction. The redox capacities of free copper, its ability to trigger the production of reactive oxygen species and the close relationships with the regulation of iron and zinc are remarkable features. Major advances in our understanding of the relationships between copper, neuronal functions and neurodegeneration have occurred these last two decades. The metabolism of copper and the current knowledge on the consequences of copper dysregulation on brain disorders are reviewed, with a focus on neurodegenerative diseases, such as Wilson’s disease, Alzheimer’s disease and Parkinson’s disease.
【 授权许可】
CC BY
© 2014 by the authors; licensee MDPI, Basel, Switzerland.
【 预 览 】
Files | Size | Format | View |
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RO202003190024857ZK.pdf | 974KB | download |