The team was also able to make human skin cells younger in the lab. Professor Juan Carlos Izpisua Belmonte from the Salk's Gene Expression Laboratory said the process would be "complex".

"It has plasticity and, with careful modulation, ageing might be reversed". In fact, data shows that the biggest risk factor for heart disease, cancer and neurodegenerative disorders is simply age. The method, called cellular reprogramming, was a breakthrough because iPSCs can divide indefinitely and becoming any cell type.

Only in the last few years have biologists come to realize that the state of the epigenome may be a major cause of aging.

The Salk team used partial reprogramming, which induced expression of Yamanaka factors for just 2 to 4 days. The right photo shows improved recovery following cellular reprogramming.

This is the first report in which cellular reprogramming extends lifespan in a live animal.

To those who are looking for the fountain of youth, you may not have to look far.

The genes have to be handled with care because the rapid cell division seen in embryos could be a hallmark of cancer in adults. Research in 2013 and 2014 found that introducing iPSCs in living animals was fatal, resulting in cancerous growths or organ failure from adult cells having lost their identity.

In the new study, the researchers devised a way to turn on the Yamanaka factors, but only for short periods of time. They turned to a rare genetic disease called progeria. The researchers also tried the technique on mice with progeria, a condition which leaves them - and humans - prematurely old.

A treatment that could turn back the ravages of time is edging closer as scientists have discovered how to "reprogram" cells to stop them growing old.

The team used DNA reprogramming methods in live mice with progeria, the premature ageing disease progeria, which also affects humans. "It is hard to say specifically why the animal lives longer", says co-first author Paloma Martinez-Redondo. "It gives us exciting insights into which pathways could be targeted to delay cellular aging". "In fact, the animals died at some point", says Ocampo. "But this study shows that ageing is a very dynamic and plastic process, and therefore will be more amenable to therapeutic interventions than we previously thought".

In mice carrying a mutation leading to premature aging, reprogramming of chemical marks in the genome, known as epigenetic marks, reduced many signs of aging in the mice and extended their lifespan on average from 18 weeks to 24. But due to the complexities of aging, any clinical trial could be up to 10 years away, they warn. IPS cells have high proliferation rates and are not yet specialized to perform functions, such as being part of the skin. These events take place within a stable environment that minimizes molecular and cellular damage. As a result, altering the way it interacts with the body may change how an organism ages.

The last decade of scientific research has dramatically improved our understanding of the aging process. "So the cells never go back to a pluripotent state". The factors must be expressed for 2 to 3 weeks for cells to reach pluripotency.