| GSTM1 null genotype as risk factor for late-onset Alzheimer's disease in Italian patients. | |
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MedLine Citation:
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PMID: 22381228 Owner: NLM Status: Publisher |
Abstract/OtherAbstract:
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Alzheimer's disease (AD) is the most common form of dementia in the elderly. The causes of AD are very complex but there is general agreement about the existence of a link between Alzheimer's disease and oxidative stress. The Glutathione S-transferases (GSTs) act to detoxify products of oxidation that cause damage to macromolecules. Particular attention has been focused on GST genes because polymorphisms are important determinants of disease risk. To evaluate if GSTA1, GSTM1, GSTP1, and GSTT1 genes are associated with LOAD we screened a case-control population (n=311). Differences in genotype distributions between AD patients and controls were found only for the GSTM1 null genotype (P<0.001). In addition, a logistic regression analysis also conferred a positive association between the GSTM1 null genotype and LOAD after adjustment for age and gender (OR=2.09; 95%CI=1.31-3.35). The GSTM1 enzyme detoxifies substances such as exogenous and endogenous metabolites and plays a regulatory role in cellular signaling. Previous studies have highlighted that GSTM1 has a role in neurodegenerative disorders, but no data have associated the GSTM1 gene with AD risk. Our outcome suggests that the GSTM1 null genotype is a risk factor for AD in Italian patients. |
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Authors:
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Sara Piacentini; Renato Polimanti; Rosanna Squitti; Mariacarla Ventriglia; Emanuele Cassetta; Fabrizio Vernieri; Paolo Maria Rossini; Dario Manfellotto; Maria Fuciarelli |
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Publication Detail:
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Type: JOURNAL ARTICLE Date: 2012-2-28 |
Journal Detail:
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Title: Journal of the neurological sciences Volume: - ISSN: 1878-5883 ISO Abbreviation: - Publication Date: 2012 Feb |
Date Detail:
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Created Date: 2012-3-2 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 0375403 Medline TA: J Neurol Sci Country: - |
Other Details:
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Languages: ENG Pagination: - Citation Subset: - |
Copyright Information:
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Copyright © 2012 Elsevier B.V. All rights reserved. |
Affiliation:
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Department of Biology, University of Rome "Tor Vergata", Rome, Italy. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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