Alzheimers 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 Aβ aggregation is not yet elucidated, age-associated disturbances of metal ion metabolism have been proposed to promote the formation of aggregates from soluble Aβ. Oxidative stress is postulated to be a downstream effect of Aβ-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/Aβ-metal ion interactions and the use of antioxidant metal chelators as potential therapy against AD.
Keywords: Amyloid beta, Alzheimer, ’, s disease, oxidative stress and ion chelators
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