New study explains how we age
A new study, published in the journal Nature, has provided significant insights into aging, opening up a "new area of understanding of how and why we age." The research involved five organisms: humans, fruit flies, rats, mice, and worms. Scientists found that aging appeared to impact cellular processes in the same way across the groups. The findings could help uncover ways to reverse aging.
Why does this story matter?
We are still uncovering new aspects of how we age and studies like the current one are contributing to a growing body of research that seeks to understand the science behind aging. This field of study has attracted massive investments over the years. Recently, a biotech start-up called Altos Labs procured $3 billion for developing a medical procedure that can reverse human aging.
Molecular processes become less reliable with aging
As we age, molecular processes within cells undergo changes, becoming less reliable. Gene mutations become more common, and the ends of chromosomes, called telomeres, break off, making them shorter. In young cells, an enzyme called telomerase keeps telomeres from wearing away too much. However, as cell division continues, there is not enough telomerase, so the telomeres grow shorter.
Many studies have investigated the effect of aging on gene-expression
Studies have investigated the effect of aging on gene expression before. However, only a few have studied how aging affects transcription, a process where genetic information is copied from a blueprint DNA strand to RNA molecules, according to Andreas Beyer, from the University of Cologne. There is an enzyme called RNA polymerase 2 (Pol 2) that directs the transcription process.
Team studied transcription changes in "very different kinds of life"
Researchers measured how aging affected the speed at which the Pol 2 enzyme moved along the DNA strand as it created the RNA copy. The team looked at genome-wide transcription changes in five "very different kinds of life," including nematode worms, fruit flies, mice, rats, and humans, at different adult ages. Genome refers to the complete set of genes in a cell.
Pol 2 enzyme became faster with age but less precise
Researchers found that on average, Pol 2 became faster with age, but less precise and became more error-prone across all of the five groups. Previous research has shown that restricting diet and inhibiting insulin signaling can delay aging and extend lifespan in many animals. So the team decided to study if these factors had an effect on the speed of Pol 2.
The enzyme moved slower in mice on a low-calorie diet
In worms, mice, and fruit flies which had mutations in insulin signaling genes, the Pol 2 enzyme moved at a slower pace. The enzyme also moved slower in mice that were on a low-calorie diet. To understand if the speed of the enzyme affected the lifespan, the team studied fruit flies and worms that carried a mutation that slowed down Pol 2.
The organisms with the mutation lived 10 to 20% longer
Interestingly, the researchers found that the fruit flies and worms, which had the mutation, were found to live 10 to 20% longer than the non-mutant ones. When the mutations were reversed, by using gene editing, in worms, their lifespans were reduced.
What are the implications of the study?
The study demonstrates how aging mechanisms are consistent across distantly related species, said Colin Selman, from the University of Glasgow. Importantly, it would also help understand how Pol 2 could be a target for drugs that aim to slow down the aging process. "There may be opportunities to effectively repurpose some of these drugs to investigate their effects on aging," said Selman.
