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Identification of 12 genetic loci associated with human healthspan. / Zenin, Aleksandr; Tsepilov, Yakov; Sharapov, Sodbo et al.

In: Communications Biology, Vol. 2, No. 1, 41, 30.01.2019, p. 41.

Research output: Contribution to journal › Article › peer-review

Harvard

Zenin, A, Tsepilov, Y, Sharapov, S, Getmantsev, E, Menshikov, LI, Fedichev, PO & Aulchenko, Y 2019, 'Identification of 12 genetic loci associated with human healthspan', Communications Biology, vol. 2, no. 1, 41, pp. 41. https://doi.org/10.1038/s42003-019-0290-0

APA

Zenin, A., Tsepilov, Y., Sharapov, S., Getmantsev, E., Menshikov, L. I., Fedichev, P. O., & Aulchenko, Y. (2019). Identification of 12 genetic loci associated with human healthspan. Communications Biology, 2(1), 41. [41]. https://doi.org/10.1038/s42003-019-0290-0

Vancouver

Zenin A, Tsepilov Y, Sharapov S, Getmantsev E, Menshikov LI, Fedichev PO et al. Identification of 12 genetic loci associated with human healthspan. Communications Biology. 2019 Jan 30;2(1):41. 41. doi: 10.1038/s42003-019-0290-0

Author

Zenin, Aleksandr ; Tsepilov, Yakov ; Sharapov, Sodbo et al. / Identification of 12 genetic loci associated with human healthspan. In: Communications Biology. 2019 ; Vol. 2, No. 1. pp. 41.

BibTeX

@article{dab2582787da4c52b93d46ba8433d94f,
title = "Identification of 12 genetic loci associated with human healthspan",
abstract = "Aging populations face diminishing quality of life due to increased disease and morbidity. These challenges call for longevity research to focus on understanding the pathways controlling healthspan. We use the data from the UK Biobank (UKB) cohort and observe that the risks of major chronic diseases increased exponentially and double every eight years, i.e., at a rate compatible with the Gompertz mortality law. Assuming that aging drives the acceleration in morbidity rates, we build a risk model to predict the age at the end of healthspan depending on age, gender, and genetic background. Using the sub-population of 300,447 British individuals as a discovery cohort, we identify 12 loci associated with healthspan at the whole-genome significance level. We find strong genetic correlations between healthspan and all-cause mortality, life-history, and lifestyle traits. We thereby conclude that the healthspan offers a promising new way to interrogate the genetics of human longevity.",
keywords = "GENOME-WIDE ASSOCIATION, LD SCORE REGRESSION, LIFE-SPAN, HUMAN LONGEVITY, VARIANTS, RISK, SUSCEPTIBILITY, METAANALYSIS, GWAS, LIMITATIONS",
author = "Aleksandr Zenin and Yakov Tsepilov and Sodbo Sharapov and Evgeny Getmantsev and Menshikov, {L. I.} and Fedichev, {Peter O.} and Yurii Aulchenko",
year = "2019",
month = jan,
day = "30",
doi = "10.1038/s42003-019-0290-0",
language = "English",
volume = "2",
pages = "41",
journal = "Communications Biology",
issn = "2399-3642",
publisher = "Springer Nature",
number = "1",

}

RIS

TY - JOUR

T1 - Identification of 12 genetic loci associated with human healthspan

AU - Zenin, Aleksandr

AU - Tsepilov, Yakov

AU - Sharapov, Sodbo

AU - Getmantsev, Evgeny

AU - Menshikov, L. I.

AU - Fedichev, Peter O.

AU - Aulchenko, Yurii

PY - 2019/1/30

Y1 - 2019/1/30

N2 - Aging populations face diminishing quality of life due to increased disease and morbidity. These challenges call for longevity research to focus on understanding the pathways controlling healthspan. We use the data from the UK Biobank (UKB) cohort and observe that the risks of major chronic diseases increased exponentially and double every eight years, i.e., at a rate compatible with the Gompertz mortality law. Assuming that aging drives the acceleration in morbidity rates, we build a risk model to predict the age at the end of healthspan depending on age, gender, and genetic background. Using the sub-population of 300,447 British individuals as a discovery cohort, we identify 12 loci associated with healthspan at the whole-genome significance level. We find strong genetic correlations between healthspan and all-cause mortality, life-history, and lifestyle traits. We thereby conclude that the healthspan offers a promising new way to interrogate the genetics of human longevity.

AB - Aging populations face diminishing quality of life due to increased disease and morbidity. These challenges call for longevity research to focus on understanding the pathways controlling healthspan. We use the data from the UK Biobank (UKB) cohort and observe that the risks of major chronic diseases increased exponentially and double every eight years, i.e., at a rate compatible with the Gompertz mortality law. Assuming that aging drives the acceleration in morbidity rates, we build a risk model to predict the age at the end of healthspan depending on age, gender, and genetic background. Using the sub-population of 300,447 British individuals as a discovery cohort, we identify 12 loci associated with healthspan at the whole-genome significance level. We find strong genetic correlations between healthspan and all-cause mortality, life-history, and lifestyle traits. We thereby conclude that the healthspan offers a promising new way to interrogate the genetics of human longevity.

KW - GENOME-WIDE ASSOCIATION

KW - LD SCORE REGRESSION

KW - LIFE-SPAN

KW - HUMAN LONGEVITY

KW - VARIANTS

KW - RISK

KW - SUSCEPTIBILITY

KW - METAANALYSIS

KW - GWAS

KW - LIMITATIONS

UR - http://www.scopus.com/inward/record.url?scp=85067212333&partnerID=8YFLogxK

U2 - 10.1038/s42003-019-0290-0

DO - 10.1038/s42003-019-0290-0

M3 - Article

C2 - 30729179

AN - SCOPUS:85067212333

VL - 2

SP - 41

JO - Communications Biology

JF - Communications Biology

SN - 2399-3642

IS - 1

M1 - 41

ER -

ID: 21346065