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pubmed-article:17183426pubmed:abstractTextClinical manifestation of Alzheimer's disease may depend upon interaction among its risk factors. Apolipoprotein E-deficient mice undergo oxidative damage and cognitive impairment when deprived of folate. We demonstrate herein that these mice were depleted in the methyl donor S-adenosyl methionine (SAM), which inhibited glutathione S-transferase, since this enzyme requires methylation of oxidative species prior to glutathione-dependent reduction. Dietary supplementation with SAM alleviated neuropathology. Since SAM deficiency promotes presenilin-1 overexpression, which increases gamma-secretase expression and Abeta generation, these findings directly link nutritional deficiency and genetic risk factors, and support supplementation with SAM for Alzheimer's therapy.lld:pubmed
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pubmed-article:17183426pubmed:articleTitleS-adenosyl methionine: A connection between nutritional and genetic risk factors for neurodegeneration in Alzheimer's disease.lld:pubmed
pubmed-article:17183426pubmed:affiliationCenter for Cellular Neurobiology and Neurodegeneration Research, Department of Biological Sciences, UMassLowell, One University Avenue, Lowell, MA 01854, USA.lld:pubmed
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