Association of GWAS Top Genes With Late-Onset Alzheimer’s Disease in Colombian Population

ABSTRACT: Objective: The association of variants in CLU, CR1, PICALM, BIN1, ABCA7, and CD33 genes with late-onset Alzheimer’s disease (LOAD) was evaluated and confirmed through genome-wide association study. However, it is unknown whether these associations can be replicated in admixed populations....

Full description

Autores:
Moreno García, Diana Jennifer
Ruíz Mendoza, Susana
Ríos Gallardo, Angela Magnolia
Lopera Restrepo, Francisco Javier
Ostos Alfonso, Henry
Marc Via, Marc
Bedoya Berrío, Gabriel de Jesús
Tipo de recurso:
Article of investigation
Fecha de publicación:
2017
Institución:
Universidad de Antioquia
Repositorio:
Repositorio UdeA
Idioma:
spa
OAI Identifier:
oai:bibliotecadigital.udea.edu.co:10495/26742
Acceso en línea:
http://hdl.handle.net/10495/26742
Palabra clave:
Polymorphism Genetic
Polimorfismo Genético
Enfermedad de Alzheimer
Alzheimer Disease
Genética
Genetics
Rights
openAccess
License
http://creativecommons.org/licenses/by/2.5/co/
Description
Summary:ABSTRACT: Objective: The association of variants in CLU, CR1, PICALM, BIN1, ABCA7, and CD33 genes with late-onset Alzheimer’s disease (LOAD) was evaluated and confirmed through genome-wide association study. However, it is unknown whether these associations can be replicated in admixed populations. Methods: The association of 14 single-nucleotide polymorphisms in those genes was evaluated in 280 LOAD cases and 357 controls from the Colombian population. Results: In a multivariate analysis using age, gender, APOEe4 status, and admixture covariates, significant associations were obtained (P < .05) for variants in BIN1 (rs744373, odds ratio [OR]: 1.42), CLU (rs11136000, OR: 0.66), PICALM (rs541458, OR: 0.69), ABCA7 (rs3764650, OR: 1.7), and CD33 (rs3865444, OR: 1.12). Likewise, a significant interaction effect was observed between CLU and CR1 variants with APOE. Conclusion: This study replicated the associations previously reported in populations of European ancestry and shows that APOE variants have a regulatory role on the effect that variants in other loci have on LOAD, reflecting the importance of gene–gene interactions in the etiology of neurodegenerative diseases.