A 13-year study looks into what drives ageing and the implications of remaining forever young…relatively speaking.
For thousands of years people have sought the powers of special fountains to help stem the ageing process. But the name linked most closely to the search for a Fountain of Youth is 16th-century Spanish explorer Juan Ponce de Leon, who allegedly thought it would be found in Florida in the United States. Try as he might to find such a powerful drop soon his will, and resources, dried up.
Fast forward to the present day and it seems as if a particular research project has opened the flow in answering what drives ageing. Reported in the global Time magazine and medical journal Cell in 2023, the findings have been made public in a study published by lead researcher Dr David Sinclair, a professor of genetics at Harvard Medical School in the United States. Put in lay terms the study describes a ground breaking discovery of an ‘ageing clock’ that can speed up, or reverse, the ageing of cells.
As reported in the article, scientists studying ageing have debated what drives the process of cells getting older. Most of the work to date has honed in on mutations in DNA. A process that can, over time, play havoc with a cell’s normal functioning and trigger the process of what is called ‘cell death’. The validity of this theory began to diminish as older people’s cells are not necessarily riddled with mutations. Moreover, animals or people harbouring a higher burden of mutated cells don’t seem to necessarily age prematurely.
Silent cells
Based on this, Dr Sinclair and his team focused on another part of the genome, called the epigenome. He postulated that as all cells have the same DNA blueprint, the epigenome is what makes skin cells turn into skin cells and brain cells into brain cells. It does this by providing different instructions to different cells for which genes to turn on, and which to keep ‘silent’.
In the Cell paper Information Theory of Ageing, Dr Sinclair and his team report that not only can they age mice on an accelerated timeline, but they can also reverse the effects of that ageing and restore some of the biological signs of youthfulness to the mice. That reversibility, says the article, establishes that the main drivers of ageing aren’t mutations to the DNA, but miscues in the genetic instructions that go off the rails.
“Underlying ageing is information that is lost in cells, not just the accumulation of damage,” he says. “That’s a paradigm shift in how to think about ageing. If the cause of ageing was because a cell became full of mutations, then age reversal would not be possible. But by showing that we can reverse the ageing process, that shows that the system is intact, that there is a backup copy and the software needs to be rebooted.”
In the mice, he and his team developed a way to reboot cells essentially erasing the corrupted signals that put the cells on the path toward ageing. They mimicked the effects of ageing on the epigenome by introducing breaks in the DNA of young mice.
