The epigenetic clock and telomere length are independently associated with chronological age and mortality

Marioni, Riccardo E., Harris, Sarah E., Shah, Sonia, McRae, Allan F., von Zglinicki, Thomas, Martin-Ruiz, Carmen, Wray, Naomi R., Visscher, Peter M. and Deary, Ian J. (2016) The epigenetic clock and telomere length are independently associated with chronological age and mortality. International Journal of Epidemiology, 45 2: 424-432. doi:10.1093/ije/dyw041

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Author Marioni, Riccardo E.
Harris, Sarah E.
Shah, Sonia
McRae, Allan F.
von Zglinicki, Thomas
Martin-Ruiz, Carmen
Wray, Naomi R.
Visscher, Peter M.
Deary, Ian J.
Title The epigenetic clock and telomere length are independently associated with chronological age and mortality
Journal name International Journal of Epidemiology   Check publisher's open access policy
ISSN 1464-3685
0300-5771
Publication date 2016-04-11
Year available 2016
Sub-type Article (original research)
DOI 10.1093/ije/dyw041
Open Access Status DOI
Volume 45
Issue 2
Start page 424
End page 432
Total pages 9
Place of publication Oxford, United Kingdom
Publisher Oxford University Press
Language eng
Abstract Telomere length and DNA methylation have been proposed as biological clock measures that track chronological age. Whether they change in tandem, or contribute independently to the prediction of chronological age, is not known.
Formatted abstract
Background: Telomere length and DNA methylation have been proposed as biological clock measures that track chronological age. Whether they change in tandem, or contribute independently to the prediction of chronological age, is not known.

Methods: We address these points using data from two Scottish cohorts: the Lothian Birth Cohorts of 1921 (LBC1921) and 1936 (LBC1936). Telomere length and epigenetic clock estimates from DNA methylation were measured in 920 LBC1936 participants (ages 70, 73 and 76 years) and in 414 LBC1921 participants (ages 79, 87 and 90 years).

Results: The epigenetic clock changed over time at roughly the same rate as chronological age in both cohorts. Telomere length decreased at 48-67 base pairs per year on average. Weak, non-significant correlations were found between epigenetic clock estimates and telomere length. Telomere length explained 6.6% of the variance in age in LBC1921, the epigenetic clock explained 10.0%, and combined they explained 17.3% (all P < 1 × 10-7). Corresponding figures for the LBC1936 cohort were 14.3%, 11.7% and 19.5% (all P < 1 × 10-12). In a combined cohorts analysis, the respective estimates were 2.8%, 28.5% and 29.5%. Also in a combined cohorts analysis, a one standard deviation increase in baseline epigenetic age was linked to a 22% increased mortality risk (P = 2.6 × 10-4) whereas, in the same model, a one standard deviation increase in baseline telomere length was independently linked to an 11% decreased mortality risk (P = 0.06).

Conclusions: These results suggest that telomere length and epigenetic clock estimates are independent predictors of chronological age and mortality risk.
Keyword Ageing
Epigenetic clock
Longitudinal
Mortality
Telomeres
Q-Index Code C1
Q-Index Status Provisional Code
Grant ID BB/F019394/1
G0601333
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
Collections: HERDC Pre-Audit
Queensland Brain Institute Publications
UQ Diamantina Institute Publications
 
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