Scientists are discovering ways to potentially slow aging in humans

Scientists are discovering ways to potentially slow aging in humans

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 mysteries that remain unsolved, most notably understanding the causes of aging and how we can slow or reverse it.

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

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

“This is the only aha moment of my life so far. I mean, that’s the kind of discovery you don’t make every other day,” said Dr. Andreas Beyer, the lead researcher, calling the results “a great discovery”.

“There’s a storm on Twitter. Some colleagues are very excited,” he told Euronews Next.

Before Beyer and his team started their research project 10 years ago, the typical aging study would “only look at differential gene expression,” says Beyer.

Previous studies, he explains, asked questions like, “As you age, which genes get turned on and which genes get turned off?” and “How does this change the regulation or metabolism in the cell?”

But no one asked how the transcription process itself changes with age, a question that could provide insights that could ultimately help us reverse or halt the decline.

Transcription, the key to healthy aging

Transcription is fundamental 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 carries the genetic information needed to make new proteins in a cell. Proteins determine the health and function of cells, and cells then structure all living things.

Our cells regenerate for a lifetime, “but every cell is different, and what makes them different are the different genes that are activated in them,” explains Beyer. “This activation is called transcription”.

Because genes give cells their purpose, their transcription must be error-free.

“You have to make the right amount of transcripts for each gene and have an exact copy of the gene sequence, but you also have to activate exactly the 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, and so on. And because each cell performs a different function, a different set of genes are activated (transcribed) in each cell type.

The “machine” – as Beyer calls it – which is responsible for producing the transcription copy of the gene sequences is called Pol II (RNA polymerase II).

And his team discovered that the transcription process speeds up with age, and this accelerated transcription causes Pol II to make more mistakes, resulting in essentially “bad” copies that can lead to numerous diseases.

“If Pol II gets too fast, it makes more mistakes, and then the sequence is no longer identical to the genome sequence. The consequences are similar to mutations in the genome itself,” says Beyer.

Stop bad cell copies

Previous research had already shown that a low-calorie diet and inhibiting insulin signaling – blocking the signal between insulin and cells – can delay aging and increase lifespan in many animals.

In their experiments, Beyer’s team wanted to find out if these had an impact in order to slow Pol II’s speed and reduce the number of bad copies.

The study — a collaborative effort involving 26 people from six different laboratories — first worked with worms, mice and fruit flies genetically engineered to inhibit insulin signaling, and mice fed a low-calorie diet to determine cell transcription performance with age . In both cases, Pol II reacted and traveled more slowly and made fewer mistakes.

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

When the researchers reversed the mutations in worms through gene editing, the animals’ lifespans shortened, establishing a causal link.

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

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

The cross-species results confirm that it’s “really a general phenomenon that applies to aging, and not just specific to the single model of, say, flies,” Beyer said.

“Our study says that, for example, a healthy diet or this calorie-restricted intervention would improve the quality of the transcription of RNA production in the cell. And that would then have long-term positive effects on the cells.” “.

The results could help prevent cancer from manifesting, Papantonis notes, since “it is a disease of advanced age due to bugs.

They may also allow us to “better understand aging, better understand what’s going on as we age,” and ultimately “better understand interventions, which I think open up new opportunities to delay aging or have a healthy one.” promote aging,” said Beyer.

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