Amyloid beta-peptide and amyloid pathology are central to the oxidative stress and inflammatory cascades under which Alzheimer's disease brain exists.
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.
Butterfield
D Allan
DA
Department of Chemistry, Center of Membrane Sciences, University of Kentucky, Lexington, KY 40506-0055, USA. dabcns@uky.edu
Griffin
Sue
S
Munch
Gerald
G
Pasinetti
Giulio Maria
GM
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
D016229:Amyloid beta-Peptides