German scientists make a ‘major discovery’ that could slow down the aging process

Despite centuries of research and advances in medicine, many mysteries remain unsolved, the main ones being understanding what causes aging and how we can slow or reverse it.

But a new study published in the scientific journal Nature may finally find answers to these questions.

Researchers from the University of Cologne in Germany found that gene transcription – the process by which a cell makes an RNA copy of a piece of DNA – not only becomes faster with age but also less precise and more prone to errors, but they also discovered that certain processes could help us reverse this decline.

“This is, so far, the only eureka moment in my life. I mean, this is a kind of discovery that you don’t make every other day,” said Dr. Andreas Meyer, the lead researcher, calling the results a “major discovery.”

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

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

Previous studies, he explains, have been asking questions like “As you age, what genes are being turned on and which genes are being turned off?” and “How does that change the regulation or metabolism in the cell?””

But no one has asked how the process of transcription itself changes as we age, a line of inquiry that could provide insights to help us reverse or stop the decline.

Transcription, the key to healthy aging

Transcription is fundamental to 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 make up the structure of all living things.

Throughout our lives, our cells regenerate, “but each cell is different, and the different genes that are activated in it are what make them different,” Beyer explains. “this action is called transcription”.

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

“You need to create the right amount of transcripts for each gene and have an exact copy of the gene sequence, but also, you need the exact genes that the cell needs to function properly,” 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, each has a different gene sequence.

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

And what his team discovered was that the transcription process becomes faster as we age, and Pol II makes more mistakes because of this accelerated transcription, which leads to essentially “bad” copies that lead to numerous diseases.

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

Stopped bad cell copies, the second big one

Previous research had already proven that low-calorie diets and inhibition of insulin signaling – blocking the signal between insulin and cells – could slow aging and extend lifespan in many animals. In their experiments, Meyer’s team tried to find out if these had any effect in slowing down the speed of Pol II and reducing the number of defective copies.

The investigation – a collaboration of 26 people across six different laboratories – worked with worms, mice and fruit flies genetically modified to inhibit insulin signaling as well as mice on a low-calorie diet to improve cell transcriptional performance in determine old age. . In both cases, Pol II responded and traveled more slowly, making fewer mistakes.

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

When the researchers used gene editing to reverse the mutations in the worms, the animals’ lifespans were shortened, establishing a causal link.

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

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

The cross-species results confirm that “aging is really a general phenomenon, and not just specific to the individual model of, for example, flies,” Beyer said.

“Our study is saying, for example, that if you put on a healthy diet or, on this caloric restriction intervention, the quality of transcription of the RNA production in the cell would be improved. And this would have beneficial effects for the cells in the long run”.

The results could help prevent cancer from manifesting, according to Papantonis, “it’s a late-life disease because of errors. Restricting errors may be a way to limit the onset of cancer or late-life disease”.

They could also allow us to “better understand aging, better understand what’s going on when we get older,” and ultimately, “better understand interventions, which opens up, in my I think new opportunities to delay aging or to expand healthy aging,” said Beyer.

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