Abstract
Human lifespan variation is mainly determined by environmental factors, whereas the genetic contribution is 25–30% and expected to be polygenic. Two complementary fields go hand in hand in order to unravel the mechanisms of biological aging: genomic and biomarker research. Explorative and candidate gene studies of the human genome by genetic, transcriptomic, and epigenomic approaches have resulted in the identification of a limited number of interesting positive linkage regions, genes, and pathways that contribute to lifespan variation. The possibilities to further exploit these findings are rapidly increasing through the use of novel technologies, such as next-generation sequencing. Genomic research is progressively being integrated with biomarker studies on aging, including the application of (noninvasive) deep phenotyping and omics data – generated using novel technologies – in a wealth of studies in human populations. Hence, these studies may assist in obtaining a more holistic perspective on the role of the genome in aging and lifespan regulation.
Highlights
Human life expectancy has increased remarkably over the last two centuries worldwide [1], it is still highly variable between countries [2]
To determine which age-related phenotypes associate with human familial longevity, the offspring of long-lived individuals, which are predisposed to longevity, can be compared to geographically- and age-matched population controls
Examples of family-based longevity studies are the Ashkenazi Jews cohort [71], GEnetics of Healthy Ageing (GEHA) study [94], Long Life Family Study (LLFS) [7], and Leiden Longevity Study (LLS) [15]
Summary
Human life expectancy has increased remarkably over the last two centuries worldwide [1], it is still highly variable between countries [2]. Age is the main risk factor for the majority of common diseases contributing to disability, reaching an old age does not necessarily result in a higher degree of age-related disability This is illustrated by the presence of long-lived individuals from families expressing exceptional longevity that may reach high ages without major disabilities [4, 5]. Their offspring – considered ‘‘decelerated’’ or ‘‘healthy agers’’ – have a lower prevalence of age-related diseases, such as cancer, cardiovascular disease, hypertension, and type 2 diabetes [6,7,8,9], compared to similaraged controls. Biomarker research is just as relevant for genomic studies of human aging as the analysis of the genome itself
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