Novel compound to delay ageing identified

Washington

Scientists have identified a compound that may delay physical ageing processes and prevent Alzheimer's and Parkinson's diseases.

As we live longer and longer, a lot of people are occupied with their state of health and, not least, quality of life in old age.

Researchers all over the world are trying to understand ageing mechanisms, as this knowledge may eventually help to postpone physical ageing and extend life.

None of the existing explanations of physical ageing are able to explain all the biological aspects of human ageing.

Previous research has shown that a main process in ageing is the capacity of the cells to keep our genes, our DNA, more or less intact.

However, changes in the cells' power stations, the mitochondria, also affect ageing processes.

Researchers from the University of Copenhagen and the National Institute of Health in the US have shown that the coenzyme NAD+ bridges the gap between two main ageing theories — repairs to the DNA and poor functioning mitochondria.

"Our new study shows an age-dependent decrease in the level of NAD+, and this decrease is far greater for organisms with early ageing and a lack of DNA repairs," said Vilhelm Bohr from the National Institute of Health.

"We were surprised to see that adding NAD+ postponed both the ageing processes of the cells and extended life in worms and in a mouse model," said Bohr.

The researchers bred mice and roundworm with the illness Ataxia telangiectasia (A-T) for the purpose of the study.

In A-T patients the part of the brain that is responsible for coordination gradually degenerates, DNA repairs are lacking, and they experience other symptoms characteristic of early ageing.

"We know from previous studies that a drop in the level of NAD+ results in metabolism errors, neurodegeneration and ageing, but the underlying mechanisms remain unclear to us," said Bohr.

"Our new study stresses that the substance NAD+ plays a main role both in maintaining the health of the cells' power stations and in their capacity for repairing the genes," he said.

The study also indicates that damage to the DNA can result in poor functioning mitochondria, and that this can lead to increasing neurodegeneration in A-T patients. Adding the substance NAD+ can stop the damage to the mitochondria.

Even though the researchers have only examined the effect of the substance on model organisms and not administered the substance to patients, they expect to see the same effect in humans, as the cell repair mechanisms are universal for the cells of all living organisms.

Understanding the universal mechanisms at cell level is key to understanding human ageing and why we become more susceptible to illness as we grow older, researchers said.

The study appears in the journal Cell Metabolism. — PTI