Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2003-4-16
pubmed:abstractText
A great amount of evidence suggests that neuroinflammation may be a major pathogenetic mechanism in the pathophysiology of sporadic Alzheimer's Disease (sAD). Recently, polymorphisms in the endothelial nitric oxide synthase (NOS3) gene have been associated to late onset Alzheimer's Disease in a British population. However, other groups failed to replicate this finding in Asiatic and Caucasian populations. We conducted a case-control study including a clinically well-defined group of 149 sAD patients and 149 age and sex matched controls to test the association between NOS3 Glu298Asp polymorphism and sAD in an ethnically homogenous Italian population. All subjects were genotyped at NOS3 and apolipoprotein E. No significant difference was found in either allele or genotype frequencies between cases and controls, even after stratification for Apolipoprotein E4 carrier status. The NOS3 Glu298Asp polymorphism does not appear to influence the risk of developing sAD in an Italian population.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0304-3940
pubmed:author
pubmed:issnType
Print
pubmed:day
8
pubmed:volume
341
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
229-32
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2003
pubmed:articleTitle
No association between Glu298Asp endothelial nitric oxide synthase polymorphism and Italian sporadic Alzheimer's disease.
pubmed:affiliation
Department of Neurology and Rehabilitation, Centre for Aging Brain and Dementia, Institute of Neuropsychiatry, University of Palermo, Italy.
pubmed:publicationType
Journal Article, Comparative Study