Oxidative stress and Alzheimer disease

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Research in the field of molecular biology has helped to provide a better understanding of both the cascade of biochemical events that occurs with Alzheimer disease (AD) and the heterogeneous nature of the disease. One hypothesis that accounts for both the heterogeneous nature of AD and the fact that aging is the most obvious risk factor is that free radicals are involved. The probability of this involvement is supported by the fact that neurons are extremely sensitive to attacks by destructive free radicals. Furthermore, lesions are present in the brains of those with AD that are typically associated with attacks by free radicals (e.g., damage to DNA, protein oxidation, lipid peroxidation, and advanced glycosylation end products), and metals (e.g., iron, copper, zinc, and aluminum) are present that have catalytic activity that produce free radicals, beta-amyloid is aggregated and produces more free radicals in the presence of free radicals; beta-amyloid toxicity is eliminated by free radical scavengers. AD has been linked to deviations in the mitochondria (supplies energy to cell) affecting cytochrome-c oxidase. These deviations may contribute to the abnormal production of free radicals. Many free radical scavengers (e.g., vitamin E, deprenyl, and ginkgo biloba extract) have produced promising results in relation to AD, as has desferrioxamine (an iron-chelating agent) and anti-inflammatory drugs and estrogens, which also have an antioxidant effect.

AMERICAN JOURNAL OF CLINICAL NUTRITION, 2000, Vol 71, Iss 2, pp 621S-629S

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