Page last updated at 17:05 GMT, Sunday, 10 August 2008 18:05 UK

Cell change 'keeps organs young'

Liver cells
Toxic proteins build up in organs over time

Researchers may have found a way to halt the biological clock which slows down our bodies over the decades.

A US team thinks it may have found the genetic levers to help boost a system vital to cleaning up faulty proteins within our cells.

The journal Nature Medicine reported that the livers of genetically-altered older mice worked as well as those in younger animals.

They suggested it might one day help people with progressive brain diseases.

These results show it's possible to correct this protein 'logjam' that occurs in our cells as we get older, thereby perhaps helping us to enjoy healthier lives well into old age
Dr Ana Maria Cuervo
Yeshiva University

The researchers, from Yeshiva University in New York, are focusing on a process which is central to the proper working of cells.

The fundamental chemicals of cells - proteins - often have very short working lives, and need to be cleared away and recycled as soon as possible.

The body has a system for doing just that, but it becomes progressively less efficient as we get older.

This leads to progressive falls in the function of major organs - the heart, liver and brain, some of which contribute to the diseases of old age.

Dr Ana Maria Cuervo, from Yeshiva, created a mouse with two genetic alterations.

The first, when activated, boosted the number of specific cell receptors linked to this protein recycling function, while the second allowed the first to be turned on whenever Dr Cuervo wished simply by modifying the animal's diet.

Switched on

She waited until the mice were six months old - the point at which age-related decline in the protein-recycling system begins - then turned on the receptor gene.

When examined at two years old, the liver cells of these mice were far more effective at recycling protein compared with normal mice.

When the overall liver function of the very old genetically-modified mice was tested, they performed at a comparable level to much younger mice.

Dr Cuervo said: "These results show it's possible to correct this protein 'logjam' that occurs in our cells as we get older, thereby perhaps helping us to enjoy healthier lives well into old age."

She now plans to test animal models of Alzheimer's and Parkinson's diseases, believing that the abnormal protein deposits in Alzheimer's in particular might be dealt with more effectively this way.

Thomas von Zglinicki, Professor of Cellular Gerontology at Newcastle University, said that the results were "very exciting".

"It's not often you see studies where they have managed to improve function in this way.

"What they seem to have managed is to maintain the mice at this young stage, and both restore and maintain normal activity."

He said that it should, in theory, be possible to achieve the same effect across the whole body.

A spokesman for the Alzheimer's Society said: "As we age we have an increase in protein misfolding and general faults in protein processing, so the ability to maintain an effective system to clear these would be beneficial.

"However, a direct line to the clearance of defective proteins in the brain is not so clear from this research."




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