Oxidative Stress in Diabetes and Alzheimer's Disease

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.

Association Between Diabetes and Hippocampal Atrophy in Elderly Japanese: The Hisayama Study

“…First, it is reported that elevated 2-h PG values are considered a good marker for oxidative stress arising from postprandial hyperglycemia (17) and correlate with insulin resistance (18). Hyperglycemia increases oxidative stress and produces advanced glycation end products, resulting in an accumulation of amyloid b-protein and neurodegeneration in the brain (2,19). In addition, in subjects with insulin resistance or hyperinsulinemia, abnormally elevated insulin levels in the brain are suggested to stimulate amyloid b-protein secretion and inhibit the extracellular degradation of amyloid b-protein by competition for insulindegrading enzyme (2).…”

Combined Exercise and Insulin-Like Growth Factor-1 Supplementation Induces Neurogenesis in Old Rats, but Do Not Attenuate Age-Associated DNA Damage

“…[1][2][3][4] It is well documented that the interaction of ROS with lipids and proteins has a significant impact on cellular function in the brain. [5][6][7][8] However, recent investigations have revealed that DNA damage/repair can contribute to the age-associated neurodegeneration. [2][3][4] Indeed, significant damage to DNA causes activation of pro-apoptotic and DNA repair proteins.…”

Role of the Neutrophil NADPH Oxidase and S100A8/A9 in the Pathophysiology of Chronic Inflammation

“…ROS production is a prominent feature in various cardiovascular-related diseases such as hypertension, atherosclerosis, and ischemic heart diseases. Moreover, it was suggested that ROS play a role in a variety of age-related diseases such as some neurological diseases like Alzheimer's disease, type 2 diabetes or even reproductive disorders (for reviews, see Kukreja & Hess, 1992;Reddy et al, 2009;Valko et al, 2007). Among this pleiad of diseases, ROS derived from the neutrophil NADPH oxidase complex (NOX2) have notably been implicated in the pathophysiology of rheumatoid arthritis, atherosclerosis, chronic obstructive inflammatory disease and inflammation-associated cancer.…”