title: Therapeutic potential in Alzheimer disease.
abstract: Oxidative damage is shown to affect every class of biological macromolecule in Alzheimer disease. Disruptions in iron and copper homeostasis are understood as being key players in neurodegenerative disease pathogenesis. Metal homeostasis as it pertains to alterations in brain function in neurodegenerative diseases is reviewed here with its relations to oxidative stress. While there is substantial documented evidence for alterations in transition metal metabolism, redox-activity and localization, it is also important to note that alterations in specific copper- and iron-containing metalloenzymes also contribute to the neurodegenerative process. 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.
authors.affiliation: Department of Pathology, Case Western Reserve University, Cleveland, Ohio 44106, USA.
authors.forename: A D
authors.initials: AD
authors.lastname: Cash
authors.forename: G
authors.initials: G
authors.lastname: Perry
authors.forename: M A
authors.initials: MA
authors.lastname: Smith
mesh_terms: D000544:Alzheimer Disease / Q000188:drug therapy / Q000209:etiology / Q000378:metabolism*; D016229:Amyloid beta-Peptides / Q000378:metabolism; D000818:Animals; D006706:Homeostasis; D006801:Humans; D008667:Metalloproteins / Q000378:metabolism / Q000502:physiology; D018384:Oxidative Stress / Q000502:physiology; D017382:Reactive Oxygen Species / Q000378:metabolism; D014131:Trace Elements / Q000378:metabolism* / Q000494:pharmacology
chemical_list: D016229:Amyloid beta-Peptides; D008667:Metalloproteins; D017382:Reactive Oxygen Species; D014131:Trace Elements