rdf:type |
|
lifeskim:mentions |
|
pubmed:issue |
6
|
pubmed:dateCreated |
2006-12-21
|
pubmed:abstractText |
Clinical 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.
|
pubmed:language |
eng
|
pubmed:journal |
|
pubmed:citationSubset |
IM
|
pubmed:chemical |
|
pubmed:status |
MEDLINE
|
pubmed:issn |
1279-7707
|
pubmed:author |
|
pubmed:issnType |
Print
|
pubmed:volume |
10
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
541-4
|
pubmed:meshHeading |
pubmed-meshheading:17183426-Adenosine,
pubmed-meshheading:17183426-Alzheimer Disease,
pubmed-meshheading:17183426-Animals,
pubmed-meshheading:17183426-Apolipoproteins E,
pubmed-meshheading:17183426-Disease Models, Animal,
pubmed-meshheading:17183426-Enzyme Inhibitors,
pubmed-meshheading:17183426-Ethionine,
pubmed-meshheading:17183426-Gene Expression Regulation, Enzymologic,
pubmed-meshheading:17183426-Glutathione Transferase,
pubmed-meshheading:17183426-Mice,
pubmed-meshheading:17183426-Mice, Knockout,
pubmed-meshheading:17183426-Oxidative Stress,
pubmed-meshheading:17183426-Risk Factors,
pubmed-meshheading:17183426-Vitamin E Deficiency
|
pubmed:articleTitle |
S-adenosyl methionine: A connection between nutritional and genetic risk factors for neurodegeneration in Alzheimer's disease.
|
pubmed:affiliation |
Center for Cellular Neurobiology and Neurodegeneration Research, Department of Biological Sciences, UMassLowell, One University Avenue, Lowell, MA 01854, USA.
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|