Discovery by Newcastle University scientists could lead to treatment for premature ageing

Ageing expert Professor Thomas von Zglinicki from Newcastle University.

Ageing expert Professor Thomas von Zglinicki from Newcastle University.

First published in News

SCIENTISTS in the North-East believe they may have found a way to predict - and eventually treat - premature ageing.

The Newcastle University researchers also believe that restricting our diet could be one way of making this happen.

Previous studies have shown that restricting calories has caused mice to live longer than normal.

Experiments, including restricting nutrients, resulted in more efficient assembly of proteins in the mitochondria – the mechanism which powers animal and human cells.

A complex mix of proteins appear to work together more effectively, while on their own they generate toxic free radicals, which in turn cause cells to age more rapidly.

If this approach works in people as well as mice it could lead to new drugs to combat premature ageing.

In a paper published in the journal Nature Communications Professor Thomas von Zglinicki, professor of cellular gerontology at the Institute for Ageing and Health, Newcastle University, said: “Free radicals have long been linked with the ageing process. Mitochondria generate the energy required to keep our bodies going but they also generate free radicals.

“How exactly they are involved in ageing is still controversial. Our data shows that quite minor differences can explain large variations in healthy lifespan.

“Essentially what we have found is that the ageing process goes slower than normal in mice that managed to form mitochondrial protein complexes more efficiently, and that we actually could help them to do so.”

At first, the team found the mitochondria from long-lived animals had fewer of the key proteins and seemed less well suited for energy production than shorter-lived mice.

However, further research showed that assembly of the protein complex was the key.

If individual components were more scarce, the assembly was perfect, but became more sloppy if more material was around.

This led to less efficient energy production and more release of free radicals, toxic by-products of mitochondrial metabolism.

Dr Satomi Miwa, joint lead researcher on the team and a specialist on mitochondrial function, said: “This goes a long way to explain how calorie restriction can improve mitochondrial function, extend lifespan and reduce or postpone many age-associated diseases.”

Prof von Zglinicki added: “What we now need to do is to see how we can improve the quality of these protein complexes in humans and whether this would extend healthy life.”


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