Immortality is something that will likely elude humans. We’re too complex and fragile to live normal lives without reaching some sort of biological terminus.

Regardless, science is quite keen on extending our lifespan, and one way in which we might do this is to ensure our genetic material deteriorates slower than it otherwise would. In effect, this is what a new study, published in the Journal of the American College of Cardiology, reports this week.

As our cells age, so do we. Although there isn’t a linear correlation between cellular aging and “actual” aging in the way we commonly measure it, the degradation of our cells is a useful proxy in this regard.

Cellular aging can be measured by looking at a person’s telomeres, the caps at the end of our chromosomes. They prevent the chromosomes from getting damaged or accidentally fusing with their neighbors, but over time, as they weaken, they shrink and contract. This makes chromosomes more vulnerable, and as they get damaged, so do we, generally speaking.

Therefore, if there was a way to lengthen telomeres, then we’d effectively reverse cellular aging in a patient. This doesn’t mean the patient is technically getting younger, but it could mean that their general aging is stalled.

A team led by the Houston Methodist Research Institute (HMRI) decided to give this a try, and succeed where other research groups have failed in the past.

^{Explaining the implications of the study. Houston Methodist via Vimeo.}

They first examined 17 children – admittedly a small sample size – suffering from progeria, a rare genetic disorder in which children appear to age incredibly rapidly. Those afflicted by it have abnormally shaped cell nuclei, among other things, and often die by the age of 13 through a stroke or heart attack.

The team noticed that 12 of these children had significantly shortened telomeres, suggesting that this is partly why their cells are aging so rapidly.

The team then took samples of cells from these patients, and using a groundbreaking technique that introduces RNA – DNA’s more primitive chemical “cousin” – into cells directly, the team stimulated them into manufacturing more telomerase.

This is a key building block protein of telomeres; its appearance ultimately had the effect of lengthening the aged cells’ telomeres. Cellular aging stalled and was effectively reversed by this procedure, if only for a few days. Previously malfunctioning and corrupted cells began to proliferate and replicate like healthy ones.

The cells were not implanted back into the patients, and this is only a proof-of-concept experiment. At this point, it cannot be said that progeria or cellular aging, in general, can be reversed in a person – but it can be in a petri dish.

It’s not immortality, or an effective treatment for progeria, but it’s a start.

It is worth pointing out that, regardless of the debate as to whether telemores are the Holy Grail of ageless living or not, that cellular aging must exist for a reason, despite the fact that it ultimately results in death. It's known as cellular senescence, and it's generally a response to DNA damage, or the increased likelihood of it occuring over time. This means that, to some degree, it's probably a somewhat counterintuitive protective measure.

Still, it can't be ignored that the number of senescent cells increase as you age, and as a recent review paper pointed out, this often correlates with an increased incidence of degenerative pathologies. It's information like this that means that experts aren't entirely clear what the biological mechanism for aging actually is, and although it is often thought that senescence first evolved to suppress the development of cancers, the jury is still out on this one.

In any case, senescence at present is seen as irreversible. You may be able to fiddle with telomeres, but you can't get senescent cells to re-enter the cell cycle. Until this is achieved, you'll have to put your dreams of living forever on hold.

[H/T: Motherboard]