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dc.contributor.authorFerguson, Amy C.
dc.contributor.authorTank, Rachana
dc.contributor.authorLyall, Laura M.
dc.contributor.authorWard, Joey
dc.contributor.authorCelis-Morales, Carlos
dc.contributor.authorStrawbridge, Rona
dc.contributor.authorHo, Frederick
dc.contributor.authorWhelan, Christopher D.
dc.contributor.authorGill, Jason M.R.
dc.contributor.authorWelsh, Paul
dc.contributor.authorAnderson, Jana J.
dc.contributor.authorMark, Patrick B.
dc.contributor.authorMackay, Daniel
dc.contributor.authorSmith, Daniel J.
dc.contributor.authorPell, J.P.
dc.contributor.authorCavanagh, Jonathan
dc.contributor.authorSattar, Naveed
dc.contributor.authorLyall, Donald
dc.date.accessioned2020-12-04T13:23:00Z
dc.date.available2020-12-04T13:23:00Z
dc.date.issued2020
dc.identifier.urihttp://repositorio.ucm.cl/handle/ucm/3319
dc.description.abstractBackground: Alzheimer's disease (AD) is a neurodegenerative condition where the underlying etiology is still unclear. Investigating the potential influence of apolipoprotein E (APOE), a major genetic risk factor, on common blood biomarkers could provide a greater understanding of the mechanisms of AD and dementia risk. Objective: Our objective was to conduct the largest (to date) single-protocol investigation of blood biomarkers in the context of APOE genotype, in UK Biobank. Methods: After quality control and exclusions, data on 395,769 participants of White European ancestry were available for analysis. Linear regressions were used to test potential associations between APOE genotypes and biomarkers. Results: Several biomarkers significantly associated with APOEɛ4 'risk' and ɛ2 'protective' genotypes (versus neutral ɛ3/ɛ3). Most associations supported previous data: for example, ɛ4 genotype was associated with elevated low-density lipoprotein cholesterol (LDL) (standardized beta [b] = 0.150 standard deviations [SDs] per allele, p < 0.001) and ɛ2 with lower LDL (b = -0.456 SDs, p < 0.001). There were however instances of associations found in unexpected directions: e.g., ɛ4 and increased insulin-like growth factor (IGF-1) (b = 0.017, p < 0.001) where lower levels have been previously suggested as an AD risk factor. Conclusion: These findings highlight biomarker differences in non-demented people at genetic risk for dementia. The evidence herein supports previous hypotheses of involvement from cardiometabolic and neuroinflammatory pathways.es_CL
dc.language.isoenes_CL
dc.rightsAtribución-NoComercial-SinDerivadas 3.0 Chile*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/3.0/cl/*
dc.sourceJournal of Alzheimer's Disease, 76(4), 1541-1551es_CL
dc.subjectAPOEes_CL
dc.subjectAlzheimer’s diseasees_CL
dc.subjectUK Biobankes_CL
dc.subjectCholesteroles_CL
dc.subjectDementiaes_CL
dc.titleAlzheimer's disease susceptibility gene Apolipoprotein E (APOE) and blood biomarkers in UK Biobank (N = 395,769)es_CL
dc.typeArticlees_CL
dc.ucm.indexacionScopuses_CL
dc.ucm.indexacionIsies_CL
dc.ucm.uripubmed.ncbi.nlm.nih.gov/32651323/es_CL
dc.ucm.doidoi.org/10.3233/JAD-200338es_CL


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Atribución-NoComercial-SinDerivadas 3.0 Chile
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