A new study inches us a little closer to understanding the aging process, how it works on a cellular level, and how it might one day be slowed down or even stopped.
Since the dawn of time, humans have wanted to live longer lives. As medical science has improved, humans have indeed extended their average lifespan.
Much of this increased longevity is due to reduced levels of infant mortality, better sanitation and public health, vast improvements in the treatment of many diseases, and vaccination.
Aside from the treatment and prevention of disease, many researchers are still picking away at the mechanisms beneath the aging process itself.
Over time, cells slowly become less active and eventually stop dividing. These are known as senescent cells. They are partly to blame for our slow but inevitable decline as we grow older.
Recently, scientists from the University of Exeter in the United Kingdom discovered a way to reverse an important aspect of aging in human cells.
The researchers were particularly interested in the activity of mitochondria, or the organelles that are famously responsible for generating a cell’s power. Their aim was to jump-start activity in the aging mitochondria. To do this, the scientists used samples of cells that line the inside of blood vessels, called endothelial cells.
They targeted splicing factors within the mitochondria. Our genes code for more than one protein, and splicing factors help decide which product a particular gene will make at any given time.
The team designed novel chemicals that specifically targeted one of two splicing factors: SRSF2 or HNRNPD. Some have previously linked these particular proteins with the cellular changes involved in aging.
The scientists designed three compounds — called AP39, AP123, and RT01 — which would deliver a minute dose of hydrogen sulfide gas to mitochondria. Earlier studies showed that hydrogen sulfide influences senescence, but exactly how it manages this was not known.
They demonstrated that this tiny quantity of gas fires up the splicing factors, giving mitochondria a boost and thereby reducing senescence.
The findings, which now appear in the journal Aging, are very encouraging. The number of senescent cells in the sample dropped by an impressive 50 percent.
Researcher Prof. Lorna Harries explains the importance of these findings, saying, “As human bodies age, they accumulate old (senescent) cells that do not function as well as younger cells. This is not just an effect of aging — it’s a reason why we age.”
She also explains how “[t]he compounds developed at Exeter have the potential to tweak the mechanisms by which this aging of cells happens.”
And these results are not just applicable to cellular aging; the implications reach much farther. Prof. Harries continues, “We used to think age-related diseases like cancer, dementia, and diabetes each had a unique cause, but they actually track back to one or two common mechanisms.”
“This research focuses on one of these mechanisms, and the findings with our compounds have potentially opened up the way for new therapeutic approaches in the future.”
“This may well be the basis for a new generation of antidegenerative drugs.”
Prof. Lorna Harries
The scientists are quick to explain that their research is not trying to prolong life no matter what; they are focused on increasing an individual’s healthy lifespan, where quality of life is preserved.
Because the study of aging is complex and still holds many mysteries, it will be some time before we finally have our hands on the elixir of life. However, as the mechanisms become clearer, treatments for a range of degenerative conditions draw ever closer.