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Neurobiol Aging. 2019 Aug 20. pii: S0197-4580(19)30291-X. doi: 10.1016/j.neurobiolaging.2019.08.013. [Epub ahead of print]

Alzheimer's disease risk SNPs show no strong effect on miRNA expression in human lymphoblastoid cell lines.

Author information

1
Lübeck Interdisciplinary Platform for Genome Analytics (LIGA), Institutes of Neurogenetics and Cardiogenetics, University of Lübeck, Lübeck, Germany; Medical Systems Biology Group, Lübeck Institute of Experimental Dermatology and Institute for Cardiogenetics, University of Lübeck, Lübeck, Germany.
2
Lübeck Interdisciplinary Platform for Genome Analytics (LIGA), Institutes of Neurogenetics and Cardiogenetics, University of Lübeck, Lübeck, Germany.
3
Lübeck Interdisciplinary Platform for Genome Analytics (LIGA), Institutes of Neurogenetics and Cardiogenetics, University of Lübeck, Lübeck, Germany; Department of Psychology, Centre for Lifespan Changes in Brain and Cognition, University of Oslo, Oslo, Norway. Electronic address: lars.bertram@uni-luebeck.de.

Abstract

The role of microRNAs (miRNAs) in the pathogenesis of Alzheimer's disease (AD) is currently extensively investigated. In this study, we assessed the potential impact of AD genetic risk variants on miRNA expression by performing large-scale bioinformatic data integration. Our analysis was based on genetic variants from 3 AD genome-wide association studies (GWASs). Association with miRNA expression was tested by expression quantitative trait locus analysis using next-generation miRNA sequencing data generated in lymphoblastoid cell lines. Although, overall, we did not identify a strong effect of AD GWAS variants on miRNA expression in this cell type, we highlight 2 notable outliers, that is, miR-29c-5p and miR-6840-5p. MiR-29c-5p was recently reported to be involved in the regulation of BACE1 and SORL1 expression. In conclusion, despite 2 exceptions, our large-scale assessment provides only limited support for the hypothesis that AD GWAS variants act as miRNA expression quantitative trait loci.

KEYWORDS:

Alzheimer's disease; GWAS; Gene expression; Genetic association; eQTLs; miRNA

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