Newcastle University scientists show damaged protein may be key to premature ageing

Experts at Newcastle University have moved a step closer to finding a way to slow down the ageing process

Mike Urwin Prof. Thomas von Zglinicki at Newcastle University Campus for Ageing and Health
Prof. Thomas von Zglinicki at Newcastle University Campus for Ageing and Health

Scientists in the North East may be a step closer to finding a way to slow down the aging process.

Newcastle University has identified that damaged protein could be one of the key aspects to premature ageing.

A team of experts found that the condition of key proteins in the mitochondria - the batteries of cells - could be used to predict, and eventually treat, premature ageing.

It was established that one way of slowing down the aging process was by restricting diet to reduce the number of calories consumed.

A study with mice identified that by using calorie restriction, a system where the cells are deprived of nutrients, rodents were able to live longer than normal.

Thomas Von Zglinicki, professor of cellular gerontology at the Institute for Ageing and Health at Newcastle University, said it was an important breakthrough as it suggested differences in lifespan due to the way the body generated cells.

He 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.”

In a complex state, proteins work together more effectively, while on their own they generate toxic free radicals, which in turn cause cells to age more rapidly. If a similar mechanism is found in people it could lead to treatments, such as new drugs to improve protein assembly.

Further research showed that assembly of the protein complex was the key.

If individual components were more scarce, the protein complex was perfect, but became more sloppy if more material was around. This then led to less efficient energy production and more release of oxygen free radicals, toxic by-products of mitochondrial metabolism.

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

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