Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
2003-5-2
pubmed:abstractText
Alzheimer's disease (AD) is a genetically complex neurodegenerative disorder and the leading cause of dementia of the elderly. Recently, Hu et al. suggested that a trinucleotide deletion in intron 13 of the APBB1 gene was a factor protecting against late-onset AD. We report here the results of a case/control study aimed at replicating this association. Our study included 461 AD patients and 397 matched controls. We compared the allele and genotype frequencies of the polymorphism between the two groups but did not find any statistically significant difference (P=0.08 and P=0.09, respectively). By contrast, adjusting for age and sex, we found a slight risk associated with the deletion (odds ratio=1.47, 95% confidence interval=1.05-2.04). Stratification by age showed that the risk effect associated with the deletion concerned subjects aged less than 65 years.
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
15
pubmed:volume
342
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
5-8
pubmed:dateRevised
2004-11-17
pubmed:meshHeading
pubmed:year
2003
pubmed:articleTitle
A risk for early-onset Alzheimer's disease associated with the APBB1 gene (FE65) intron 13 polymorphism.
pubmed:affiliation
Aventis Pharma, Evry Genetics Center & Neurodegenerative Disease Group, Paris Research Center, 13 Quai Jules Guesde, 94400, Vitry-sur-Seine, France.
pubmed:publicationType
Journal Article