Abstract
Alzheimer disease is characterized by oxidative damage to every class of biological macromolecule. Disruptions in iron and copper homeostasis are implicated as having key roles in neurodegenerative disease pathogenesis. Metal homeostasis as it pertains to alterations in brain function and its relation to oxidative stress in neurodegenerative diseases is reviewed here. While there is documented evidence for alterations in transition metal metabolism, redox-activity and localization, it is important to note that alterations in specific copper- and ironcontaining metalloenzymes contribute to the neurodegeneration in AD. Understanding these changes offers the opportunity to identify pathways where modification of the disease process can offer effective clinical intervention, from gene therapy to pharmaceuticals with antioxidant and chelating properties.
Keywords: neurodegeneration, mitochondria, free radicals, iron
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