title: Amyloid beta-peptide and amyloid pathology are central to the oxidative stress and inflammatory cascades under which Alzheimer's disease brain exists.
abstract: Alzheimer's disease (AD) brain is characterized by excess deposition of amyloid beta-peptide (Abeta), particularly the 42-amino acid peptide [Abeta(1-42)] and by extensive oxidative stress. Several sources of the oxidative stress and inflammatory cascades are likely, including that induced by advanced glycation end products, microglial activation, and by Abeta(1-42) and its sequelae. This review briefly examines each of these sources of oxidative stress and inflammation in AD brain and discusses their potential roles in the clinical progression of AD dementia.
authors.affiliation: Department of Chemistry, Center of Membrane Sciences, University of Kentucky, Lexington, KY 40506-0055, USA. dabcns@uky.edu
authors.forename: D Allan
authors.initials: DA
authors.lastname: Butterfield
authors.forename: Sue
authors.initials: S
authors.lastname: Griffin
authors.forename: Gerald
authors.initials: G
authors.lastname: Munch
authors.forename: Giulio Maria
authors.initials: GM
authors.lastname: Pasinetti
mesh_terms: D000210:Acute-Phase Reaction / Q000473:pathology*; D000544:Alzheimer Disease / Q000473:pathology*; D016229:Amyloid beta-Peptides / Q000378:metabolism*; D000686:Amyloidosis / Q000473:pathology*; D000818:Animals; D001921:Brain / Q000473:pathology; D006801:Humans; D018384:Oxidative Stress / Q000502:physiology*; D012307:Risk Factors
chemical_list: D016229:Amyloid beta-Peptides