title: Role of metal dyshomeostasis in Alzheimer's disease.
abstract: Despite serving a crucial purpose in neurobiological function, transition metals play a sinister part in the aging brain, where the abnormal accumulation and distribution of reactive iron, copper, and zinc elicit oxidative stress and macromolecular damage that impedes cellular function. Alzheimer's disease (AD), an age-related neurodegenerative condition, presents marked accumulations of oxidative stress-induced damage, and increasing evidence points to aberrant transition metal homeostasis as a critical factor in its pathogenesis. Amyloid-β oligomerization and fibrillation, considered by many to be the precipitating factor underlying AD onset and development, is also induced by abnormal transition metal activity. We here elaborate on the roles of iron, copper, and zinc in AD and describe the therapeutic implications they present.
authors.affiliation: Department of Pathology, Case Western Reserve University, Cleveland, Ohio, USA. Xiongwei.zhu@case.edu.
authors.forename: David J
authors.initials: DJ
authors.lastname: Bonda
authors.forename: Hyoung-gon
authors.initials: HG
authors.lastname: Lee
authors.forename: Jeffrey A
authors.initials: JA
authors.lastname: Blair
authors.forename: Xiongwei
authors.initials: X
authors.lastname: Zhu
authors.forename: George
authors.initials: G
authors.lastname: Perry
authors.forename: Mark A
authors.initials: MA
authors.lastname: Smith
mesh_terms: D000544:Alzheimer Disease / Q000188:drug therapy / Q000378:metabolism*; D000818:Animals; D002614:Chelating Agents / Q000627:therapeutic use; D003300:Copper / Q000378:metabolism*; D006801:Humans; D007501:Iron / Q000378:metabolism*; D015032:Zinc / Q000378:metabolism*
chemical_list: D002614:Chelating Agents; D003300:Copper; D007501:Iron; D015032:Zinc