Source:http://linkedlifedata.com/resource/pubmed/id/12664314
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rdf:type | |
lifeskim:mentions |
umls-concept:C0002395,
umls-concept:C0017337,
umls-concept:C0021760,
umls-concept:C0031928,
umls-concept:C0063717,
umls-concept:C0079189,
umls-concept:C0333348,
umls-concept:C0441889,
umls-concept:C0442805,
umls-concept:C0679058,
umls-concept:C1274040,
umls-concept:C1547699,
umls-concept:C1704240,
umls-concept:C1749467,
umls-concept:C1882417,
umls-concept:C2700640
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pubmed:issue |
1
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pubmed:dateCreated |
2003-3-28
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pubmed:abstractText |
Interleukin-6 (IL-6) is a multifunctional cytokine involved in the pathogenesis of Alzheimer's disease (AD). The effects of IL-6 are mediated through a specific receptor complex made up of a ligand binding glycoprotein (gp80 or IL-6R) and a signal transducing glycoprotein (gp130). Conflicting results have been reported concerning altered IL-6 or soluble IL-6R (sIL-6R) levels in serum and CSF in AD. This study investigated whether genetic heterogeneity determines the magnitude of the difference in IL-6 and sIL-6R levels in AD. Fifty-eight AD patients and 25 control subjects were included. Plasma and CSF IL-6 and sIL-6R levels were measured and the IL-6 variable number of number repeats ( IL-6vntr) and IL-6 promoter ( IL-6prom) genotypes were determined. sIL-6R levels in plasma and CSF were higher in AD patients than in control subjects. This elevation was striking among non-carriers of the IL-6vntr*C allele and among subjects homozygous for the IL-6prom*C allele whereas no difference in plasma and CSF sIL-6R levels was observed among carriers of the IL-6vntr*C allele and among subjects with the IL-6prom*CG and IL-6prom*GG genotypes. We conclude that plasma and CSF levels of sIL-6R are significantly increased in AD patients and that the magnitude of increase is determined by the IL-6 genotype.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
0940-1334
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pubmed:author |
pubmed-author:BürgerKatharinaK,
pubmed-author:BagliMetinM,
pubmed-author:BeckerKarinK,
pubmed-author:HampelHaraldH,
pubmed-author:HeunReinhardR,
pubmed-author:JessenFrankF,
pubmed-author:MöllerHans-JürgenHJ,
pubmed-author:MaierWolfgangW,
pubmed-author:PapassotiropoulosAndreasA,
pubmed-author:PtokUU,
pubmed-author:RaoMarie LuiseML
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pubmed:issnType |
Print
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pubmed:volume |
253
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
44-8
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pubmed:dateRevised |
2009-5-11
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pubmed:meshHeading |
pubmed-meshheading:12664314-Aged,
pubmed-meshheading:12664314-Alzheimer Disease,
pubmed-meshheading:12664314-Biological Markers,
pubmed-meshheading:12664314-Case-Control Studies,
pubmed-meshheading:12664314-Female,
pubmed-meshheading:12664314-Genotype,
pubmed-meshheading:12664314-Humans,
pubmed-meshheading:12664314-Interleukin-6,
pubmed-meshheading:12664314-Male,
pubmed-meshheading:12664314-Pilot Projects,
pubmed-meshheading:12664314-Polymorphism, Genetic,
pubmed-meshheading:12664314-Receptors, Interleukin-6,
pubmed-meshheading:12664314-Solubility
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pubmed:year |
2003
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pubmed:articleTitle |
Polymorphisms of the gene encoding the inflammatory cytokine interleukin-6 determine the magnitude of the increase in soluble interleukin-6 receptor levels in Alzheimer's disease. Results of a pilot study.
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pubmed:affiliation |
Department of Psychiatry, University of Bonn, Venusberg, 53105 Bonn, Germany.
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, Non-U.S. Gov't
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