Oxidative stress in diabetes and Alzheimer's disease

J Alzheimers Dis. 2009;16(4):763-74. doi: 10.3233/JAD-2009-1013.

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.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Alzheimer Disease / drug therapy
  • Alzheimer Disease / physiopathology*
  • Animals
  • Antioxidants / chemistry
  • Antioxidants / pharmacology
  • Antioxidants / therapeutic use
  • Diabetes Mellitus / drug therapy
  • Diabetes Mellitus / physiopathology*
  • Humans
  • Oxidative Stress / drug effects
  • Oxidative Stress / physiology*

Substances

  • Antioxidants