The research linked below is an example of work in the Longevity Dividend model: study the comparative genetics of longevity in humans to find epigenetic patterns and genetic variants that correlate with membership of long-lived families. From there proceed to identify underlying mechanisms and undertake drug development to find ways to recreate those differences. This mainstream, well-supported research is absolutely the wrong path to take if the aim is to producing meaningful extension of healthy life, however. Aging occurs because we accumulate damage as a side-effect of metabolism within and around our cells. Outside of a few rare and devastating genetic mutations, we all suffer exactly the same types of damage for exactly the same reasons. Genetic and epigenetic variants have a limited effect on our interaction with this growing damage until very old age, so we should ignore them: researchers should focus instead on repairing and reverting these known forms of damage that cause aging. The resulting treatments built for this purpose will be applicable to everyone, and thus can be mass produced cheaply.
Given a choice between spending vast sums on building age-slowing drugs that help maintain people for longer in a state of being old and damaged, or building repair biotechnologies that help maintain people in a youthful, undamaged state, I know in which direction my money is heading. Drugs to slow aging will never be particularly helpful for those already old and damaged, while repair biotechnologies will aid those in greatest need of repair. It seems fairly self-evident to me where the focus should be. Yet the vast majority of research funding for the comparatively young field of longevity science is aimed at the inferior goal of slowing aging. This must change.
Frailty is a common condition associated with old age, characterized by weight loss, weakness, decreased activity level and reduced mobility, which together increase the risk of injury and death. Yet, not all elderly people become frail; some remain vigorous and robust well into old-age. The question remains: why? "People who are frail are more vulnerable to serious complications from falls or surgery and more susceptible to infection. Understanding why some elderly people do not experience a loss of balance or strength and do not suffer from abnormal gait may help us prevent and treat such physical decline."
The new project taps into the resources of [the] LonGenity Research Study, which builds upon the Longevity Genes Project, an ongoing 15-year study with more than 500 Ashkenazi Jews over the age of 95. LonGenity compares the genetics of the centenarians and their children with those with usual survival. Over the past 10 years, [researchers have] identified several biological markers that may explain their extreme longevity. "We have shown that our centenarian participants have a significant genetic advantage over the general population. Their rare genetic variants have allowed them to live longer, healthier lives and avoid or significantly delay age-related diseases, such as Alzheimer's and type 2 diabetes. We now want to know if a family history of those same 'longevity genes' reduces the risk for frailty."
The researchers will build on a pilot study funded by the American Federation for Aging Research that linked exceptional longevity to improved physical function and reduced risk of frailty. [The] team plans to further those initial efforts to identify gene variants that keep frailty at bay, explore biological pathways that may lead to frailty, and develop drugs that mimic the effect of those frailty-preventing genes.