Mark my words. When the first real treatment happens people will change their tune. They need to see it work and see that it’s safe.

A new study of about 900 U.S. adults has found that only 33% would use a hypothetical life extension treatment that would allow them “to live forever,” even if it were available today. About 42% said they would not use it, and 25% said they were unsure.

The study, published by University of Texas researchers Michael Barnett and Jessica Helphrey, appeared in the Journal of Aging Studies on April 21.

To keep the longevity train rolling it may not be enough to cure diseases. We may also need to address the underlying condition of aging itself, which is, after all, the primary risk factor for late-life decline.

What happens if we slow down aging?

Aging is associated with an overall decline in health and increased frailty, and is a major risk factor for multiple chronic diseases. Frailty syndrome, characterized by weakness, fatigue and low physical activity, affects more than 30% of the elderly population. Increasing our understanding of the mechanisms underlying the aging process is a top priority to facilitate the development of interventions that will lead to the preservation of health and improvements on survival and lifespan.

Cumulative evidence suggests that diet and metabolism are key targetable regulators of healthy lifespan. Prof. Haim Cohen, Director of the Sagol Healthy Human Longevity Center at Bar-Ilan University, focuses much of his research on the SIRT6 protein that is involved in regulating many biological processes, such as aging, obesity, and insulin resistance.

In a study just published in the journal Nature Communications, an international team led by Cohen and his Ph.D. student Asael Roichman—together with Prof. Rafael de Cabo, of the National Institute on Aging at the National Institutes of Health, Prof. Manuel Serrani, of the Institute for Research in Biomedicine in Barcelona, and Prof. Eyal Gottlieb from the Technion—report that transgenic mice express high levels of the SIRT6 gene, and show that their life expectancy can be increased by an average of 30% in both males and females. Translated into human terms this means that a 90-year-old could live until nearly 120!

A new discovery could lead to new drugs for faster repairing muscles after injury — or rebuilding muscle mass lost during the normal aging process.

Researchers at the Salk Institute have uncovered a mechanism by which stem cells can help regenerate muscles. The discovery could provide a new drug target for repairing muscles after injury or rebuilding muscle mass lost during the normal aging process.

The breakthrough started with a set of proteins called Yamanaka factors, which have long been studied as a key part of stem cell therapy. These factors are used to convert regular cells – most commonly skin cells – into what are known as induced pluripotent stem cells (iPS), which can then go on to differentiate into a variety of other cell types. That in turn helps regenerate tissue. But exactly how the Yamanaka factors worked their magic remained a mystery.

“Our laboratory previously showed that these factors can rejuvenate cells and promote tissue regeneration in live animals,” says Chao Wang, first author of the study. “But how this happens was not previously known.”