Interdisciplinary bio-hacking team finds genetic stability key to turning off ageing

A group of scientists led a life extension world record holder has determined that stabilising gene networks is key to switching off the process of ageing.

The team, from Hong Kong-based biohacking company Gero, comprises experts from a vast array of different scientific backgrounds, alongside Professor Robert J Shmookler Reis, the current world record holder in life extension for model animals, and has just published research on the subject in the journal Scientific Reports.

“In our work, we analyzed the stability of a simple gene network model and found that gene networks describing most common species are inherently unstable,” explained Dr Peter Fedichev, CSO of Gero.

“Over time, it undergoes exponential accumulation of gene regulation deviations leading to diseases and death.

“We conjectured, that the instability is the cause of aging. However, should the repair systems be sufficiently effective, the gene network can stabilize so that the damage to the gene regulation can remain constrained along with mortality of the organism.”

mole-rat

This theory is supported by the genetic networks of animals that do not experience a decline in function or a rise in mortality as they get older. The team gave the example of naked mole rats, which are negligibly senescent – ie they barely age – and have highly stress-resistant tissue due to the stability of their gentic networks.

By contrast, humans’ genetic networks are very unstable, resulting in a decline in human tissue’s ability to reproduce, regenerate and resist stress, resulting in our increase in mortality and decline in function as we age.

These differences are caused by a small number of major factors, including how effective genes are connected as a network, the rate DNA repairs itself, the turnover of proteome – the proteins expressed by a gene – and genome size, and the team at Gero believes that lifespan can be altered by ‘hacking’ any of these aspects.

This has already been achieved in a type of worm – C. elegans – creating a lifespan ten times the norm with a single gene mutation, and it is thought that it can be achieved in other creatures with further work.

The genes of the worm C. elegans were successfully altered to significantly improve its lifespan.

The genes of the worm C. elegans were successfully altered to significantly improve its lifespan.

Gero is working with the intention of creating anti-ageing treatments, and believes that this approach is key to creating such therapeutics.

“We want to create a drug that will significantly extend a healthy and happy human life,” said the company on their website.

“The relation between stresses, stress resistance and aging is analyzed and demonstrates that damage to gene regulation from stresses encountered even at a very young age can persist for a very long time and influence lifespan,” explained the company in a media release to accompany the publication of the research.

“That is why we believe that further research into the relation between gene network stability and aging will make it possible to create entirely new therapies with potentially strong and lasting effect against age-related diseases and aging itself.”

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Stronger in old age: Stem cell research paves way for muscle-building medication

It could in the future be possible to take medication that will allow you to build muscle, even when you are in old age.

This is due to the findings of research at the Karolinska Institutet in Sweden, which found that large, and wholly unexpected, amounts of mutations in muscle stem cells blocks their ability to regenerate cells.

“What is most surprising is the high number of mutations. We have seen how a healthy 70-year-old has accumulated more than 1,000 mutations in each stem cell in the muscle, and that these mutations are not random but there are certain regions that are better protected,” said Maria Eriksson, professor at the Department of Biosciences and Nutrition at Karolinska Institutet.

With this knowledge, researchers could develop therapies that would encourage such regeneration, and so allow older people to rebuild lost muscle.

“We can demonstrate that this protection diminishes the older you become, indicating an impairment in the cell’s capacity to repair their DNA. And this is something we should be able to influence with new drugs,” explained Eriksson.

The landmark research, which is published today in the journal Nature Communications, involved the use of single stem cells, which were cultivated to provide enough DNA for whole genome sequencing – a medical first for this part of the body.

“We achieved this in the skeletal muscle tissue, which is absolutely unique. We have also found that there is very little overlap of mutations, despite the cells being located close to each other, representing an extremely complex mutational burden,” said study first author Irene Franco, a postdoc in Eriksson’s research group.

While a significant step, the research is now being expanded to look at whether exercise affects the number of mutations – a potentially vital factor in understand why and how these mutations occur.

“We aim to discover whether it is possible to individually influence the burden of mutations. Our results may be beneficial for the development of exercise programmes, particularly those designed for an ageing population,” said Eriksson.

The research is one of a host of projects being conducted across the world that have potential impacts on ageing, an area that was long ignored by much of the scientific community, but is now garnering increased support.

If many – or even a fair minority – of these findings eventually become the basis of therapeutics, it could be transformative for old age in the future, allowing people to remain healthier for far later in life and potentially even leading to longer life expectancies.