Linked Life Data

12231449

Source:http://linkedlifedata.com/resource/pubmed/id/12231449

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2002-9-16
pubmed:abstractText
According to the oxidative stress hypothesis which has been proposed as one of a number of possible mechanisms underlying pathogenesis of Alzheimer's disease (AD), accumulation of hydrogen peroxide in the brain of affected individuals, due to overproduction and/or insufficient detoxification, can trigger a cascade of neurotoxic events, thus contributing to the neuronal damage characteristic of the disease. The upregulation of enzymes that are able to neutralize hydrogen peroxide (catalase, peroxidases) would then be conceivably able to offer at least some protection from the damaging effects of this agent. In this study we examined the distribution of a functional polymorphism in the gene for catalase, -262C-->T, in an independent population of 137 AD patients and 130 control individuals. The presence of the polymorphism, which results in the elimination of a SmaI restriction site, was tested with a PCR amplification/SmaI digestion-based assay. No significant difference has emerged from the comparison of either genotype or allele frequencies (P>0.5). We conclude that the catalase gene -262C-->T polymorphism does not confer a protective effect with respect to AD.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0304-3940
pubmed:author
pubmed:issnType
Print
pubmed:day
20
pubmed:volume
330
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
210-3
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
2002
pubmed:articleTitle
An association study of a functional catalase gene polymorphism, -262C-->T, and patients with Alzheimer's disease.
pubmed:affiliation
Department of Pharmacology, School of Medicine, Aristotle University, Thessaloniki 54124, Greece.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.