Scientists discover a way to potentially slow down human aging

A new study from Germany may have found answers to age-old questions: What drives aging and what can we do to reverse it?

Despite centuries of research and advances in medicine, there are still many unsolved mysteries, chief among them understanding what causes aging and how we can slow or reverse it.

But a new study by a group of German scientists, published in the scientific journal Nature, may have finally found the answers to these questions.

Researchers from the University of Cologne in Germany have not only found that gene transcription — the process by which a cell makes an RNA copy of a DNA strand — becomes faster with age, but less accurate and more error-prone; they also discovered that certain processes could help us reverse this decline.

“So far this is the only eureka moment in my life. I mean, this is the kind of discovery you don’t make every other day,” said lead researcher Dr. Andreas Beyer, calling the findings a “significant. discovery.”

“There is a storm on Twitter. Some colleagues are very upset,” he told Euronews Next.

Before Beyer and his team began their investigative project 10 years ago, a typical aging study would “just look at differential gene expression,” says Beyer.

He explains that previous studies asked questions like, “As you age, which genes are turned on and which genes are turned off?” and “How does it change regulation or metabolism in the cell?”

But no one asked how the process of transcription itself changes as we age. It’s a line of inquiry that could provide insights that could ultimately help us reverse or stop the recession.

Transcription, the key to healthy aging

Transcription is central to Beyer’s research because it is the process by which a cell makes an RNA copy of a piece of DNA.

This copy is important because it contains the genetic information needed to make new proteins in the cell. Proteins determine the health and function of cells, and cells then structure all living things.

Throughout our lives, our cells renew themselves, “but every cell is different, and what makes them different is the different genes that are activated in them,” Beyer explains. “This activation is called transcription”.

Because genes give cells their purpose, their transcription must be perfect.

“You have to make the right amount of transcripts for each gene and have an exact copy of the gene sequence, but also activate the exact genes that the cell needs to function as it should,” Beyer said.

There are many different types of cells in the human body: nerve cells, muscle cells, blood cells, skin cells, etc. And because each cell performs a different function, a different set of genes is activated (transcribed) in each cell type.

The “machine” – as Beyer calls it – that is responsible for making transcriptional copies of gene sequences is called Pol II (RNA polymerase II).

And his team discovered that the process of transcription becomes faster as we age, and this accelerated transcription causes Pol II to make more mistakes, resulting in essentially “bad” copies that can lead to many diseases.

“If Pol II becomes too fast, it makes more mistakes, and then the sequence is no longer identical to the sequence of the genome. The consequences are similar to those that occur when there are mutations in the genome itself,” said Beyer.

Stopping bad cell copies

Previous studies had already shown that low-calorie diets and inhibition of insulin signaling – blocking the signal between insulin and cells – could delay aging and extend the lifespan of many animals.

In their experiments, Beyer’s team sought to see if they had any effect on slowing down Pol II and reducing the number of damaged copies.

The investigation — a collaboration of 26 people in six different labs — first used worms, mice and fruit flies genetically modified to inhibit insulin signaling, as well as mice on a low-calorie diet to measure the cells’ transcriptional performance in old age. . In both cases, Paul II reacted and traveled more slowly, making fewer mistakes.

Beyer and his team then tracked the survival of fruit flies and worms that carried a mutation that slowed Pol II, and the animals lived 10 to 20 percent longer than their nonmutant counterparts.

When researchers used gene editing to change the worms’ mutations, the animals’ lifespans were shortened, establishing a causal relationship.

To test their experiment on humans, they worked with blood samples from young and old individuals.

“And when we compared the young cells with very old cells in vitro, we got exactly the same results,” one of the principal investigators, Argiris Papantonis, told Euronews Next.

The cross-species findings confirm that this is “a really general phenomenon related to aging, and not just specific to one model of, say, flies,” Beyer said.

“Our study says that, for example, a healthy diet or this calorie restriction intervention will improve the transcriptional quality of RNA production in the cell. And this will have a beneficial effect on the cells in the long term.”.

Discoveries can help prevent cancer, Papantonis notes, because “it’s a late disease because of mistakes. Limiting mistakes may be a way to limit cancer or late diseases.”

They may also allow us to “better understand aging, better understand what happens when we age,” and ultimately “better understand interventions that I think open up new opportunities to delay aging or extend healthy aging,” Beyer said.

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