| pubmed-article:17900622 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:17900622 | lifeskim:mentions | umls-concept:C0002395 | lld:lifeskim |
| pubmed-article:17900622 | lifeskim:mentions | umls-concept:C0017337 | lld:lifeskim |
| pubmed-article:17900622 | lifeskim:mentions | umls-concept:C1704675 | lld:lifeskim |
| pubmed-article:17900622 | lifeskim:mentions | umls-concept:C1367477 | lld:lifeskim |
| pubmed-article:17900622 | lifeskim:mentions | umls-concept:C0683481 | lld:lifeskim |
| pubmed-article:17900622 | pubmed:issue | 1-2 | lld:pubmed |
| pubmed-article:17900622 | pubmed:dateCreated | 2007-12-7 | lld:pubmed |
| pubmed-article:17900622 | pubmed:abstractText | A chronic inflammatory process with activation of microglial cells contribute to the neurodegeneration associated with Alzheimer's disease (AD). CD14 and LXRbeta are receptors involved in the regulation of inflammatory responses of microglia in response to bacterial infection or lipopolysaccharide stimulation. In a case-control study in 266 AD patients and 273 healthy controls, we examined whether the combined gene effects between CD14 (-260) polymorphism and LXRbeta (intron 5) polymorphism might be responsible for susceptibility to AD. Subjects carrying both the CD14 (-260) C/C and the LXRbeta (intron 5) G/G genotypes had a six times lower risk of developing AD than subjects without these risk genotypes (OR 0.16, 95% CI 0.04-0.67, p=0.01). These data support a role for innate immune response genes in risk for AD. | lld:pubmed |
| pubmed-article:17900622 | pubmed:language | eng | lld:pubmed |
| pubmed-article:17900622 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17900622 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:17900622 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:17900622 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:17900622 | pubmed:issn | 0022-510X | lld:pubmed |
| pubmed-article:17900622 | pubmed:author | pubmed-author:FRISCHKORNC... | lld:pubmed |
| pubmed-article:17900622 | pubmed:author | pubmed-author:MateoIgnacioI | lld:pubmed |
| pubmed-article:17900622 | pubmed:author | pubmed-author:InfanteJonJ | lld:pubmed |
| pubmed-article:17900622 | pubmed:author | pubmed-author:BercianoJoséJ | lld:pubmed |
| pubmed-article:17900622 | pubmed:author | pubmed-author:Sánchez-Quint... | lld:pubmed |
| pubmed-article:17900622 | pubmed:author | pubmed-author:Rodríguez-Rod... | lld:pubmed |
| pubmed-article:17900622 | pubmed:author | pubmed-author:Sánchez-JuanP... | lld:pubmed |
| pubmed-article:17900622 | pubmed:author | pubmed-author:García-Gorost... | lld:pubmed |
| pubmed-article:17900622 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:17900622 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:17900622 | pubmed:volume | 264 | lld:pubmed |
| pubmed-article:17900622 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:17900622 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:17900622 | pubmed:pagination | 97-9 | lld:pubmed |
| pubmed-article:17900622 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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| pubmed-article:17900622 | pubmed:year | 2008 | lld:pubmed |
| pubmed-article:17900622 | pubmed:articleTitle | Interaction between CD14 and LXRbeta genes modulates Alzheimer's disease risk. | lld:pubmed |
| pubmed-article:17900622 | pubmed:affiliation | Neurology Service, University Hospital Marqués de Valdecilla (University of Cantabria), Santander, Spain. | lld:pubmed |
| pubmed-article:17900622 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:17900622 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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