Affiliations: [a] Department of Chemistry, Center of Membrane Sciences, and Sanders-Brown Center on Aging, University of Kentucky, Lexington, KY 40506-0055, USA | [b] Donald W. Reynolds Department of Geriatrics, GRECC, VAMC, Little Rock, AR 72205, USA | [c] Neuroimmunological Cell Biology, Interdisciplinary Center of Clinical Research (IZKF) Leipzig, 04103 Leipzig, Germany | [d] Mount Sinai School of Medicine, Neuroinflammation Research Center, Department of Psychiatry, Mount Sinai School of Medicine, New York, NY 10089, USA
Correspondence:
[*]
Corresponding author: Professor D. Allan Butterfield, Department of Chemistry, Center of Membrane Sciences, and Sanders-Brown Center on Aging, University of Kentucky, Lexington, KY 40506-0055, USA. Tel.: +1 859 257 3184; Fax: +1 859 257 5876; E-mail: dabcns@uky.edu.
Abstract: Alzheimer's disease (AD) brain is characterized by excess deposition of amyloid β-peptide (Aβ), particularly the 42-amino acid peptide [Aβ(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 Aβ(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.
