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Int J Mol Sci. 2019 Jun 21;20(12). pii: E3032. doi: 10.3390/ijms20123032.

Exploring the Relationship of Relative Telomere Length and the Epigenetic Clock in the LipidCardio Cohort.

Author information

1
Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin and the Berlin Institute of Health, Lipid Clinic at the Interdisciplinary Metabolism Center, 13353 Berlin, Germany. verena-laura.banszerus@charite.de.
2
Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin and the Berlin Institute of Health, Lipid Clinic at the Interdisciplinary Metabolism Center, 13353 Berlin, Germany. valentin.vetter@charite.de.
3
Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin and the Berlin Institute of Health, Lipid Clinic at the Interdisciplinary Metabolism Center, 13353 Berlin, Germany. bastian.salewsky@gmx.de.
4
Medizinische Klinik mit Schwerpunkt Nephrologie und Intensivmedizin, Charité-Universitätsmedizin Berlin, 13353 Berlin, Germany. koenig.maximilian@charite.de.
5
Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin and the Berlin Institute of Health, Lipid Clinic at the Interdisciplinary Metabolism Center, 13353 Berlin, Germany. ilja.demuth@charite.de.
6
Berlin-Brandenburg Center for Regenerative Medicine (BCRT), Charité Universitätsmedizin Berlin, 13353 Berlin, Germany. ilja.demuth@charite.de.

Abstract

Telomere length has been accepted widely as a biomarker of aging. Recently, a novel candidate biomarker has been suggested to predict an individual's chronological age with high accuracy: The epigenetic clock is based on the weighted DNA methylation (DNAm) fraction of a number of cytosine-phosphate-guanine sites (CpGs) selected by penalized regression analysis. Here, an established methylation-sensitive single nucleotide primer extension method was adapted, to estimate the epigenetic age of the 1005 participants of the LipidCardio Study, a patient cohort characterised by high prevalence of cardiovascular disease, based on a seven CpGs epigenetic clock. Furthermore, we measured relative leukocyte telomere length (rLTL) to assess the relationship between the established and the promising new measure of biological age. Both rLTL (0.79 ± 0.14) and DNAm age (69.67 ± 7.27 years) were available for 773 subjects (31.6% female; mean chronological age= 69.68 ± 11.01 years; mean DNAm age acceleration = -0.01 ± 7.83 years). While we detected a significant correlation between chronological age and DNAm age (n = 779, R = 0.69), we found neither evidence of an association between rLTL and the DNAm age (β = 3.00, p = 0.18) nor rLTL and the DNAm age acceleration (β = 2.76, p = 0.22) in the studied cohort, suggesting that DNAm age and rLTL measure different aspects of biological age.

KEYWORDS:

Berlin Aging Study II (BASE-II); DNA methylation (DNAm) age; DNAm age acceleration; LipidCardio Study; aging; biological age; biomarker of ageing; epigenetic clock; telomere length

PMID:
31234328
PMCID:
PMC6628615
DOI:
10.3390/ijms20123032
[Indexed for MEDLINE]
Free PMC Article

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