Copper imbalance and oxidative stress in neurodegeneration.
Much experimental evidence demonstrates that the increased production of free radicals and oxidative damage due to alterations in copper homeostasis (because of either deficit or excess or aberrant coordination of the metal) are involved in the neurodegenerative processes occurring in many disorders of the central nervous system. This review outlines the systems that are involved in copper homeostasis and in the control of copper redox reactivity. The mechanisms underlying neurodegeneration in the acknowledged genetic disturbances of copper homeostasis, namely Menkes' and Wilson's diseases, and the involvement of copper in the aetiology of the major neurodegenerative disease of the aging brain, Alzheimer's disease, will be described, with particular focus on oxidative stress.
Rossi
Luisa
L
Department of Biology, "Tor Vergata" University of Rome, Italy. luisa.rossi@uniroma2.it
Arciello
Mario
M
Capo
Concetta
C
Rotilio
Giuseppe
G
D000544:Alzheimer Disease / Q000209:etiology; D016229:Amyloid beta-Peptides / Q000502:physiology; D001921:Brain / Q000378:metabolism / Q000502:physiology*; D027682:Cation Transport Proteins / Q000502:physiology; D003300:Copper / Q000172:deficiency / Q000378:metabolism*; D006527:Hepatolenticular Degeneration / Q000209:etiology; D006706:Homeostasis / Q000502:physiology*; D006801:Humans; D007706:Menkes Kinky Hair Syndrome / Q000209:etiology; D019636:Neurodegenerative Diseases / Q000503:physiopathology*; D018384:Oxidative Stress / Q000502:physiology*; D011328:Prions / Q000502:physiology; D013482:Superoxide Dismutase / Q000235:genetics
D016229:Amyloid beta-Peptides; D027682:Cation Transport Proteins; D011328:Prions; D003300:Copper; D013482:Superoxide Dismutase