Antioxidants as a potential therapy against age-related neurodegenerative diseases: amyloid Beta toxicity and Alzheimer's disease.
Alzheimer's disease (AD) is a progressive age-related neurodegenerative disorder with distinct neuropathological features. Extracellular plaques, consisting of aggregated amyloid peptides of 39-43 amino acids are one of the most prominent pathological hallmarks of this disease. Although the exact neurochemical effector mechanism of Abeta aggregation is not yet elucidated, age-associated disturbances of metal ion metabolism have been proposed to promote the formation of aggregates from soluble Abeta. Oxidative stress is postulated to be a downstream effect of Abeta-metal ion interactions. Therefore, the modulation of brain metal metabolism and attenuation of oxidative stress by antioxidant molecules are proposed as a potential therapeutic intervention in AD. Here, we summarize the recent literature focused on APP/Abeta-metal ion interactions and the use of antioxidant metal chelators as potential therapy against AD.
Hajieva
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Institute of Physiological Chemistry & Pathobiochemistry, Johannes Gutenberg University of Mainz, Medical School, Germany.
Behl
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C
D000375:Aging / Q000502:physiology*; D000544:Alzheimer Disease / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology; D016229:Amyloid beta-Peptides / Q000378:metabolism; D000818:Animals; D000975:Antioxidants / Q000627:therapeutic use*; D006801:Humans; D019636:Neurodegenerative Diseases / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology
D016229:Amyloid beta-Peptides; D000975:Antioxidants