Affiliations: [a] Department of Chemistry, Missouri University of Science and Technology, Rolla, MO, USA | [b] Department of Pathology, Case Western Reserve University, Cleveland, OH, USA | [c] College of Sciences, University of Texas at San Antonio, San Antonio, TX, USA
Correspondence:
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Corresponding authors: V. Prakash Reddy, Department of Chemistry, Missouri University of Science and Technology, Rolla, MO 65409, USA. Tel.: +1 573 341 4768; Fax: +1 573 341 6033; E-mail: preddy@mst.edu. Mark A. Smith, Department of Pathology, Case Western Reserve University, Cleveland, OH 44106, USA. Tel.: +1 216 368 3670; Fax: +1 216 368 8964; E-mail: mark.smith@case.edu.
Note: [] Handling Editor: Ralph N. Martins
Abstract: Oxidative stress plays a major role in diabetes as well as in Alzheimer's disease and other related neurological diseases. Intracellular oxidative stress arises due to the imbalance in the production of reactive oxygen/reactive nitrogen species and cellular antioxidant defense mechanisms. In turn, the excess reactive oxygen/reactive nitrogen species mediate the damage of proteins and nucleic acids, which have been shown to have direct and deleterious consequences in diabetes and Alzheimer's disease. Oxidative stress also contributes to the production of advanced glycation end products through glycoxidation and lipid peroxidation. The advanced glycation end products and lipid peroxidation products are ubiquitous to diabetes and Alzheimer's disease and serve as markers of disease progression in both disorders. Antioxidants and advanced glycation end products inhibitors, either induced endogenously or exogenously introduced, may counteract with the deleterious effects of the reactive oxygen/reactive nitrogen species and thereby, in prevention or treatment paradigms, attenuate or substantially delay the onset of these devastating pathologies.
Keywords: Advanced glycation end products, AGE inhibitors, Alzheimer's disease, diabetes, glycation, Maillard reaction, oxidative stress, protein crosslinks
