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dc.rights.licensehttp://creativecommons.org/licenses/by/4.0es_MX
dc.creatorDANIRA TORAL RIOSes_MX
dc.creatorDIANA KARINA FRANCO BOCANEGRAes_MX
dc.creatorOSCAR ROSAS CARRASCOes_MX
dc.creatorFRANCISCO JAVIER MENA BARRANCOes_MX
dc.creatorRosa Carvajal Garcíaes_MX
dc.creatorMARCO ANTONIO MERAZ RIOSes_MX
dc.creatorVICTORIA CAMPOS PEÑAes_MX
dc.date2015
dc.date.accessioned2019-04-10T18:27:44Z
dc.date.available2019-04-10T18:27:44Z
dc.identifier.urihttp://repositorio.inger.gob.mx/jspui/handle/20.500.12100/17165
dc.descriptionAbstract: amyloid peptide is able to promote the activation of microglia and astrocytes in Alzheimer’s disease (AD), and this stimulates the production of pro-inflammatory cytokines. Inflammation contributes to the process of neurodegeneration and therefore is a key factor in the development of AD. Some of the most important proteins involved in AD inflammation are: clusterin (CLU), complement receptor 1 (CR1), C reactive protein (CRP), tumor necrosis factor α (TNF-α), the interleukins 1α (IL-1α), 6 (IL-6), 10 (IL-10) and cyclooxygenase 2 (COX-2). In particular, COX-2 is encoded by the prostaglandin-endoperoxide synthase 2 gene (PTGS2). Since variations in the genes that encode these proteins may modify gene expression or function, it is important to investigate whether these variations may change the developing AD. The aim of this study was to determine whether the presence of polymorphisms in the genes encoding the aforementioned proteins is associated in Mexican patients with AD. Fourteen polymorphisms were genotyped in 96 subjects with AD and 100 controls; the differences in allele, genotype and haplotype frequencies were analyzed. Additionally, an ancestry analysis was conducted to exclude differences in genetic ancestry among groups as a confounding factor in the study. Significant differences in frequencies between AD and controls were found for the single-nucleotide polymorphism (SNP) rs20417 within the PTGS2 gene. Ancestry analysis revealed no significant differences in the ancestry of the compared groups, and the association was significant even after adjustment for ancestry and correction for multiple testing, which strengthens the validity of the results. We conclude that this polymorphism plays an important role in the development of the AD pathology and further studies are required, including their proteins.es_MX
dc.formatAdobe PDFes_MX
dc.languageenges_MX
dc.publisherFrontiers Mediaes_MX
dc.relationhttps://www.frontiersin.org/articles/10.3389/fncel.2015.00148/fulles_MX
dc.relation.requiresSies_MX
dc.rightsAcceso Abiertoes_MX
dc.sourceFrontiers in Cellular Neuroscience (1662-5102) vol. 9 (2015)es_MX
dc.subjectBIOLOGÍA Y QUÍMICAes_MX
dc.subjectCiencias de la vidaes_MX
dc.subjectNeurocienciases_MX
dc.subjectNeuroquímicaes_MX
dc.subjectEnfermedades del sistema nervioso centrales_MX
dc.subjectEnfermedades cerebraleses_MX
dc.subjectDemenciaes_MX
dc.subjectAlzheimer, Enfermedad dees_MX
dc.subjectEnzimases_MX
dc.subjectComplejos multienzimáticoses_MX
dc.subjectSíntesis de prostagladina-endoperóxidoes_MX
dc.subjectNeuroscienceses_MX
dc.subjectNeurochemistryes_MX
dc.subjectCentral nervous system diseaseses_MX
dc.subjectBrain diseaseses_MX
dc.subjectDementiaes_MX
dc.subjectAlzheimer diseasees_MX
dc.subjectEnzimeses_MX
dc.subjectMultienzime complexeses_MX
dc.subjectProstagladin-endoperoxide synthaseses_MX
dc.titleEvaluation of inflammation-related genes polymorphisms in mexican with Alzheimer’s disease: a pilot studyes_MX
dc.typeArtículoes_MX
dc.audienceResearcherses_MX
dc.creator.idTORD870714MOCRSN08es_MX
dc.creator.idFABD880213MOCRCN04es_MX
dc.creator.idROCO750722HDFSRS05es_MX
dc.creator.idMEBF720730HDFNRR06es_MX
dc.creator.idCA1225063es_MX
dc.creator.idMERM601206HDFRSR09es_MX
dc.creator.idCAPV690409MDFMXC03es_MX
dc.creator.nameIdentifiercurpes_MX
dc.creator.nameIdentifiercurpes_MX
dc.creator.nameIdentifiercurpes_MX
dc.creator.nameIdentifiercurpes_MX
dc.creator.nameIdentifiercaes_MX
dc.creator.nameIdentifiercurpes_MX
dc.creator.nameIdentifiercurpes_MX


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