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Cytokine IL‐1 beta but not IL‐1 alpha promoter polymorphism is associated with Alzheimer disease in a population from the Canary Islands, Spain
Author(s) -
DénizNaranjo M. C.,
MuñozFernandez C.,
AlemanyRodríguez M. J.,
PérezVieitez M. C.,
AladroBenito Y.,
IruritaLatasa J.,
SánchezGarcía F.
Publication year - 2008
Publication title -
european journal of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.881
H-Index - 124
eISSN - 1468-1331
pISSN - 1351-5101
DOI - 10.1111/j.1468-1331.2008.02252.x
Subject(s) - genotype , promoter , apolipoprotein e , allele , medicine , disease , beta (programming language) , polymorphism (computer science) , population , immunology , genetics , gene , biology , gene expression , environmental health , computer science , programming language
Aims: Previous studies have reported the presence of low‐grade inflammation in Alzheimer disease (AD). Based on these data, our work attempts to investigate the effects of some promoter polymorphisms of pro‐inflammatory cytokines [interleukin (IL)‐1 alpha and IL‐1 beta] on AD. Patients and methods: A PCR‐RFLP technique was used to analyze the promoter polymorphisms of both IL‐1 alpha (−889 C/T) and IL‐1 beta (−511 C/T) and the APOE genotype from the DNA samples of 282 patients (according to NINCDS‐ADRDA criteria) and 312 control subjects. Results: (i) The risk of developing AD in our population was associated with the IL‐1 beta (−511 C/T) promoter polymorphism; (ii) such risk was independent of the risk factor allele in the APOE gene (APOE4); and (iii) the IL‐1 alpha promoter polymorphism (−889 C/T) was not associated with the disease. Conclusion: In our population, IL‐1 beta promoter polymorphism (−511 C/T) is an independent risk factor for AD.