GROWING BODY OF EVIDENCE suggests that oxidative processes may be involved in the etiology of Alzheimer disease (AD). 1 Accumulated damage to lipid membranes and DNA by oxygen free radicals and reactive oxygen species is thought to disrupt normal cell functioning and lead to neuronal death. 2 Antioxidant nutrients, including vitamin E, vitamin C, and beta carotene, are among the body's natural defense mechanisms against oxidative stress. The antioxidant nutrients have been shown through animal and laboratory studies of brain tissue to decrease lipid peroxidation 3-11 and the oxidation of proteins, 12,13 inhibit the production of reactive oxygen species, 6,14,15 prevent mitochondrial dysfunction 12,16 and DNA fragmentation, 6,17 and reduce neurotoxicity, 18,19 apoptosis, 15,19-21 and neuronal death. 18,22 Few studies have examined the relation between dietary intake of antioxidant nutrients and the development of AD. Two prospective studies 23,24 that reported on the association of vitamin E and vitamin C supplement use and AD yielded conflicting results, but both had limited power to test the hypothesis, and neither had dietary information. We report on the association between incident AD and intake of antioxidant nutrients from foods and supplements in a large community study, the Chicago Health and Aging Project (CHAP).
High intake of unsaturated, unhydrogenated fats may be protective against Alzheimer disease, whereas intake of saturated or trans-unsaturated (hydrogenated) fats may increase risk.
Background: Dietary intake of fish and the -3 fatty acids have been associated with lower risk of Alzheimer disease and stroke.Objective: To examine whether intakes of fish and the -3 fatty acids protect against age-related cognitive decline.
The results suggest that various tocopherol forms rather than alpha- tocopherol alone may be important in the vitamin E protective association with Alzheimer disease.
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