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dc.rights.licenseopenen_US
hal.structure.identifierBordeaux population health [BPH]
dc.contributor.authorANDRE, Perrine
hal.structure.identifierBordeaux population health [BPH]
dc.contributor.authorSAMIERI, Cecilia
dc.contributor.authorBUISSON, C.
hal.structure.identifierBordeaux population health [BPH]
dc.contributor.authorDARTIGUES, Jean- François
dc.contributor.authorHELMER, Catherine
dc.contributor.authorLAUGERETTE, F.
hal.structure.identifierBordeaux population health [BPH]
dc.contributor.authorFEART-COURET, Catherine
ORCID: 0000-0002-7959-1610
IDREF: 08195848X
dc.date.accessioned2020-05-06T14:39:08Z
dc.date.available2020-05-06T14:39:08Z
dc.date.issued2019
dc.identifier.issn1875-8908 (Electronic) 1387-2877 (Linking)en_US
dc.identifier.urihttps://oskar-bordeaux.fr/handle/20.500.12278/7497
dc.description.abstractEnBACKGROUND: Identifying the mechanisms involved in the pathogenesis of Alzheimer's disease (AD) remains crucially important. Chronic age-related low-grade inflammation is considered to be one such mechanism, although its causes are unclear. Lipopolysaccharide (LPS)-type endotoxins, a major component of the outer membrane of Gram-negative bacteria, are known as potent pro-inflammatory molecules. Therefore, we hypothesized that greater exposure to circulating LPS, potentially mediated by the inflammatory pathway, would be a key step of the onset of AD. OBJECTIVE: The aim of this study was to investigate the link between plasma endotoxin-exposure, inflammation, and AD. METHODS: Applying a nested case-control design, we evaluated the associations among baseline plasma endotoxin-exposure (assessed by measuring LPS-binding protein (LBP) and soluble cluster of differentiation-14 (sCD14) levels), inflammation (assessed by measuring interleukin-6 (IL6) levels), and the odds of developing AD over 12 years. Selected from a population-based cohort, 212 incident cases of AD were matched with 424 controls without dementia with regard to age, gender, and education level. RESULTS: After adjusting for a large set of confounders, including the use of anti-inflammatory drugs, only higher LBP levels were significantly associated with a 30% higher odds ratio of developing AD over 12 years (OR 1.30, 95% CIs [1.07-1.59]), regardless of IL6 levels. CONCLUSION: This large case-control study provides preliminary results concerning plasma endotoxin-exposure among the elderly and suggests that higher LBP levels, an acute-phase reactant involved in the pro-inflammatory response to LPS, are associated with higher odds of developing AD.
dc.language.isoENen_US
dc.subject.enLEHA
dc.subject.enSEPIA
dc.title.enLipopolysaccharide-Binding Protein, Soluble CD14, and the Long-Term Risk of Alzheimer's Disease: A Nested Case-Control Pilot Study of Older Community Dwellers from the Three-City Cohort
dc.title.alternativeJ Alzheimers Disen_US
dc.typeArticle de revueen_US
dc.identifier.doi10.3233/JAD-190295en_US
dc.subject.halSciences du Vivant [q-bio]/Santé publique et épidémiologieen_US
dc.identifier.pubmed31450497en_US
bordeaux.journalJournal of Alzheimer's diseaseen_US
bordeaux.page751-761en_US
bordeaux.volume71en_US
bordeaux.hal.laboratoriesBordeaux Population Health Research Center (BPH) - U1219en_US
bordeaux.issue3en_US
bordeaux.institutionUniversité de Bordeauxen_US
bordeaux.teamLEHA_BPH
bordeaux.peerReviewedouien_US
bordeaux.inpressnonen_US
hal.exportfalse
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