Scientists discover high levels of a protein in people over 85 that may slow aging – and boosting the compound in mice made them live LONGER
- Scientists found a protein called REST that suppresses over-activity of neurons in the brain
- In the brains of people who had died from ages 60 to older than 100, those who lived to at least 85 had higher levels of REST
- Experiments conducted in mice and worms showed that suppressing REST led to higher neural activity and earlier death
A fountain of youth drug could be on the horizon after the discovery of a brain protein that extends lifespan, a new study suggests.
Scientists say the protein, known as REST, slows the aging process by suppressing over-activity of neurons in the brain.
Past studies have linked excessive brain activity to memory and attention problems and disorders including dementia and epilepsy.
A study of the brains of people who had died between ages 60 and older than 100 found that individuals who were younger when they died had lower levels of REST.
Experiments then conducted in mice and worms found that blocking it led to higher neural activity and earlier deaths, but boosting it had the opposite effect.
The team, from Harvard Medical School in Cambridge, Massachusetts, says a drug that targets REST could be the secret to warding off age-associated diseases and be an anti-aging method for humans.
A new study from Harvard Medical School has found that a protein, known as REST, extends lifespan by blocking over-activity of neurons in the brain, which has been linked to early death (file image)
Previous studies have suggested the nervous system plays a role in aging, but the mechanisms were not well understood.
For the new study, published in the journal Nature, the team looked at donated brain tissue from hundreds of people who died between ages 60 and older than 100.
None of the participants had been diagnosed with any age-related brain diseases, such as dementia.
Next, they analyzed gene expression patterns, which is the extent to which various genes are turned ‘on and off’ like a light switch.
Researchers found that the participants who had lived the longest – aged 85 and older – had less expression of genes that are linked to neural excitation, which is when there is over-activity of neurons in the brain.
The team decided to conduct experiments in genetically altered mice, along with the analysis of the brain tissue, to determine if the lack of neural excitation was occurring alongside other factors directly affecting life span or if excitation was the main factor.
When they blocked REST in the animals, their neurons kicked into overdrive and then animals died sooner.
But when they dialed up REST, the mice’s neurons calmed down – and they lived longer.
Taken together, the super-agers’ high REST levels and the direct effects of turning the protein’s expression up or down on the longevity of mice suggested something remarkable: REST might cause us to live longer or shorter lives.
Developing a drug that targets REST may be the key to helping humans live longer, the authors say.
‘Strategies that boost REST levels and reduce excitatory neural activity could be used to influence aging,’ said senior author Dr Bruce Yankner, a professor of genetics at Harvard Medical School.
‘An intriguing aspect of our findings is that something as transient as the activity state of neural circuits could have such far-ranging consequences for physiology and lifespan.’
Dr Nektarios Tavernarakis, a professor of molecular systems biology who studies aging at the University of Crete, says it now seems overall neural excitation is the key to lifespan.
He added that REST might also boost longevity by preventing age-related neurological disorders.
‘Indeed, accumulating evidence couples neural over-excitation to Alzheimer’s disease,’ said Dr Tavernarakis, who was not involved in the study.
‘So REST and other molecules that control neural excitability are possible targets for interventions aimed at battling the decline and maladies of old age.’
For future research, the team says it wants to examine if neural activity is affected by genetic and/or environmental causes.