Giving mice a protein boost can increase their life expectancy by as much as 30 percent and make them less susceptible to cancer, a new study finds.
The supply of protein SIRT6, which has been found to decrease with age in some mammals, was given to 250 mice by a team from Bar-Illan University in Ramat Gan, Israel.
They found that the mice that received the protein boost had a longer life expectancy, a more youthful appearance and were therefore less prone to cancer.
Lead author Haim Cohen said it could one day work in humans, and if it does, average life expectancy could increase to nearly 120, compared to the current 80.
They haven’t tested it on humans and haven’t confirmed that it will work on humans, but the lab is trying to find drugs that can safely boost SIRT6 in humans.
“The mechanism by which the protein SIRT6 acts as a ‘fountain of youth’ allows old mice to perform the same level of vigorous activity as their young counterparts, without becoming vulnerable,” says Cohen.
Giving mice a protein boost can increase their life expectancy by as much as 30 percent and make them less susceptible to cancer, a new study finds. stock image
The supply of protein SIRT6, which has been found to decrease with age in some mammals, was given to 250 mice by a team from Bar-Illan University in Ramat Gan, Israel. stock image
AVERAGE LIFE EXPECTATION AROUND THE WORLD
- Japan – 84.3 years
- Australia – 83 years
- France 82.5 years
- Canada – 82.2 years
- UK – 81.4 years
- USA – 78.5 years
- Somalia – 56.6 years
- World – 73.3 years
- Europe – 78.2 years
- Western Pacific – 77.7 years
- America – 77.2 years
- Southeast Asia – 71.4 years
- Eastern Mediterranean – 69.7 years
- Africa – 64.5 years
Increased frailty and overall health decline are major issues associated with aging, with age being a major risk factor in several chronic diseases.
More than 30 percent of the elderly population worldwide suffers from ‘vulnerability syndrome’, which includes weakness, fatigue and low physical activity.
“Increasing our understanding of the mechanisms underlying the aging process is a top priority to facilitate the development of interventions that will lead to the maintenance of health and improvement of survival and longevity,” says Cohen.
He has focused his research on the SIRT6 protein, which controls many biological functions, such as aging, obesity and even insulin resistance.
When studying mice, the team found that high levels of the SIRT6 gene led to improvements in life expectancy — up to 30 percent more than in normal mice.
In addition, the mice showed significant improvement in overcoming a variety of age-related diseases, such as cancer and blood disorders.
In addition, they were remarkably able to perform the same level of vigorous activity as young mice and did not become weak.
Then, using a variety of biochemical methods and metabolic analyses, the researchers deciphered the mechanism by which SIRT6 acts as a sort of ‘fountain of youth’, enabling healthy aging.
They found that unenhanced older animals lose their ability to generate energy if they don’t have access to external energy sources, making them more vulnerable.
When they gave mice the boost in SIRT6, they were able to maintain the energy-generating capacity from other forms of storage, such as the breakdown of fats.
“Overall, SIRT6 controls longevity and ability to generate energy during times of limited availability, such as physical activity, fasting and aging,” they said.
‘These pathways, together with SIRT6’s known regulatory role of the major aging-related metabolic signaling pathways, position SIRT6 as a master regulator of healthy aging.’
They said this means the protein has the potential to one day become a target to maintain function in the body and delay the onset of frailty from aging.
“The mechanism by which the protein SIRT6 acts as a ‘fountain of youth’ allows old mice to perform the same level of vigorous activity as their young counterparts, without becoming vulnerable,” says Cohen. stock image
SIRT6 triggered a physical response identical to longevity diets.
“This discovery, combined with our previous findings, shows that SIRT6 controls the rate of healthy aging,” said Professor Cohen.
“If we can determine how to activate it in people, we can extend life, and that could have huge health and economic implications.”
Today, Cohen’s lab is developing methods to extend a healthy life based on these findings, which were published in the journal nature communication.
“These findings show that SIRT6 optimizes energy homeostasis in old age to delay frailty and maintain healthy aging,” they wrote.
HOW CAN SCIENTISTS USE TELOMERASE TO REVERSE THE AGING PROCESS?
Scientists have decoded an enzyme that would halt the aging of plants, animals and humans as part of a recent breakthrough study.
Unraveling the structure of the complex enzyme called telomerase could lead to drugs that slow or block the aging process, along with new treatments for cancer, researchers reported in April in the journal Nature.
Delighted scientists announced the completion of a 20-year quest to map the enzyme thought to prevent aging by repairing the ends of chromosomes.
“It took a long time,” lead researcher Kathleen Collins, a molecular biologist at the University of California at Berkeley, said in a statement.
“Our findings provide a structural framework for understanding human telomerase disease mutations and represent an important step towards telomerase-related clinical therapies.”
Part protein and part RNA (genetic material that relays instructions for building proteins) telomerase works on microscopic sheaths known as telomeres, which cover the ends of the chromosomes found in all cells.
In humans, each cell contains 23 pairs of chromosomes, including one pair of sex chromosomes — the “X” and “Y” — that differ between males and females.
Australian-American biologist Elizabeth Blackburn, who received the 2009 Nobel Prize in Medicine for discovering telomeres and their protective function in the 1970s, compared them to the tiny plastic caps that keep shoelaces from fraying.
Eventually, however, shoelace ends and telomeres break: Every time a cell divides, the telomeres wear out a little more, until the cell stops dividing and dies. This, biologists agree, is likely central to the natural aging process.