Tech UPTechnologyThey solve the mystery of why we grow old

They solve the mystery of why we grow old

Scientists from the Institute of Molecular Biology in Mainz (Germany) have made a great advance in understanding the origin of the aging process, as they have discovered that the genes belonging to a process called autophagy – an essential phase for cell renewal – promote health and fitness in young worms , but they drive the aging process in later periods.

This research thus offers us some of the first clear evidence of how the aging process arises, almost as an evolutionary quirk . These findings may also have broader implications for the treatment of neurodegenerative disorders such as Alzheimer’s, Parkinson’s, and Huntington’s disease, where autophagy is involved.

The experts demonstrated in an experiment with worms, that by promoting longevity through the closure of autophagy, there was a strong improvement in the health of the entire neuronal and mobile body in older worms.

As Charles Darwin explained at the time, natural selection leads to individuals better suited to a given environment in order to survive the race and pass on their genes to the next generation . The more fruitful a trait that promotes reproductive success, the stronger the selection for that trait.

 

Following this theory, natural selection should give rise to individuals with traits that prevent aging since their genes could be transmitted almost continuously, ensuring the transmission of genes to subsequent generations. However, we are facing an evolutionary contradiction that has been theorized since the 19th century.

 

In 1953 George C. Williams provided an interesting hypothesis that aging could appear evolutionarily in a population if certain genes promote reproductive success in youth, but then have negative effects on aging (antagonistic pleiotropy) ; that is, as long as the negative effects of the mutations that promote aging occur after the reproductive stage, evolution runs a thick veil in the face of these consequences on longevity.

 

In short, if a genetic mutation results in more offspring, but shortens life span, that’s fine.

 

Although this theory had been demonstrated mathematically and its implications demonstrated in the real world, there was no scientific evidence to support it. Up to now.

 

“These antagonistic pleiotropy genes had not been found before because it is incredibly difficult to work with old animals. We were the first to figure out how to do this on a large scale,” says Jonathan Byrne, co-author of the work.

 

By analyzing only 0.05% of the worm genome, the scientists found 30 genes that operate antagonistically (so there must be many, many more). These are the first confirmed genes that promote aging uniquely and specifically in old worms.

 

The experts were able to go back to the source of these pro-aging signals, locating them in neural tissue. Trying to turn off these genes in adult worms produced a strong improvement in neuronal status and the health of the whole body in general, which extended the life of the worms by up to 50%.

 

“Imagine getting to the middle of your life and getting a drug that leaves you as fit and mobile as someone half your age living longer – that’s what it’s like for worms,” says Thomas Wilhelm, co-author. of the study.

 

Although the authors don’t yet know the exact mechanism that causes neurons to stay healthy longer, this finding could have real implications.

 

Could we stop aging in humans with an autophagy drug?

 

Referencia: Thomas Wilhelm et al, Neuronal inhibition of the autophagy nucleation complex extends life span in post-reproductive C. elegans, Genes & Development (2017). DOI: 10.1101/gad.301648.117

 

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