As the tools of genetic analysis improve by leaps and bounds, the cost falling with each advance, more and more research is taking place into genetic influences on human longevity. This is an enormously complex area of study, and has little to no relevance to any repair-based methodology for lengthening human life. Outside the field of regenerative medicine, most aging researchers do not work on repair strategies such as SENS, however. Meanwhile there is plenty of funding for genetic studies of all sorts - compared with comparatively little available for initiatives to repair the biochemical damage of aging.
This is a sad state of affairs, but it is what it is: one of the numerous things we must help to change in the years ahead if we are to see significant progress towards engineered longevity in our lifetimes.
In any case, here is a good (and open access) example of the sort of genetic longevity studies presently taking place: detailed associations and commonalities are being uncovered in the genomes of long-lived people, and there is a lively debate over just how important any individual longevity-associated genetic variants are likely to be.
Centenarians often reach old age with delayed onset or absence of geriatric diseases ... This correlation between exceptional longevity and healthy aging suggests that common genetic factors may underlie both traits.
Estimates of the heritability of normal human lifespan range from 10% to 58%, averaging about 25%. The genetic contribution to lifespan grows markedly after age 60, indicating the heritability of exceptional longevity may be substantially higher than these estimates. The relative survival probability for siblings of centenarians increases steadily with age, until male and female siblings have a 17-fold and 8-fold increased chance, respectively, of reaching age 100 compared to others from their birth cohort. Moreover, while natural lifespan is likely a complex trait controlled by many genes with small effect sizes, extreme longevity may be determined by fewer genes of stronger effect.
To map the [genetic] loci conferring a survival advantage, we performed the second genomewide linkage scan on human longevity and the first using a high-density marker panel of single nucleotide polymorphisms. By systematically testing a range of minimum age cutoffs in 279 families with multiple long-lived siblings, we identified [multiple longevity-associated loci].
The present phase of research is producing mountains of data, and there will likely be thousands of combinations of gene-variants that have statistically significant effects on human longevity. But none of this will have the slightest impact on how long you and I live: if our lives are made longer, it will be through the use of technologies to repair and reverse the known biochemical changes that drive degenerative aging, not through genetic manipulation.
Boyden, S., & Kunkel, L. (2010). High-Density Genomewide Linkage Analysis of Exceptional Human Longevity Identifies Multiple Novel Loci PLoS ONE, 5 (8) DOI: 10.1371/journal.pone.0012432