Researchers in Japan have found that human aging may be able to be delayed or even reversed, at least at the most basic level of human cell lines. In the process, the scientists from the University of Tsukuba also found that regulation of two genes is related to how we age.
The new findings challenge one of the current popular theories of aging, that lays the blame for humans’ inevitable downhill slide with mutations that accumulate in our mitochondrial DNA over time. Mitochondrion are sometimes likened to a cellular “furnace” that produces energy through cellular respiration. Damage to the mitochondrial DNA results in changes or mutations in the DNA sequence that build up and are associated with familiar signs of aging like hair loss, osteoporosis and, of course, reduced lifespan.
So goes the theory, at least. But the Tsukuba researchers suggest that something else may be going on within our cells. Their research indicates that the issue may not be that mitochondrial DNA become damaged, but rather that genes get turned “off” or “on” over time. Most intriguing, the team led by Professor Jun-Ichi Hayashi was able to flip the switches on a few genes back to their youthful position, effectively reversing the aging process.
The researchers came to this conclusion by comparing the function level of the mitochondria in fibroblast cell lines from children under 12 years of age to those of elderly people between 80 and 97. As expected, the older cells had reduced cellular respiration, but the older cells did not show more DNA damage than those from children. This discovery led the team to propose that the reduced cellular function is tied to epigenetic regulation, changes that alter the physical structure of DNA without affecting the DNA sequence itself, causing genes to be turned on or off. Unlike mutations that damage that sequence, as in the other, aforementioned theory of aging, epigenetic changes could possibly be reversed by genetically reprogramming cells to an embryonic stem cell-like state, effectively turning back the clock on aging.
For a broad comparison, imagine that a power surge hits your home’s electrical system. If not properly wired, irreversible damage or even fire may result. However, imagine another home in which the same surge trips a switch in this home’s circuit breaker box. Simply flipping that breaker back to the “on” position should make it operate as good as new. In essence, the Tsukuba team is proposing that our DNA may not become fried with age as previously thought, but rather simply requires someone to access its genetic breaker box to reverse aging.
To test the theory, the researchers found two genes associated with mitochondrial function and essentially experimented with turning them on or off. In doing so, they were able to create defects or restore cellular respiration. These two genes regulate glycine, an amino acid, production in mitochondria, and in one of the more promising findings, a 97-year-old cell line saw its cellular respiration restored after the addition of glycine for 10 days.
The researchers’ findings were published this month in the journal Scientific Reports.
Whether or not this process could be a potential fountain of youth for humans and not just human fibroblast cell lines still remains to be seen, with much more testing required. However, if the theory holds, glycine supplements could one day become a powerful tool for life extension.
Similar research from the Salk Institute has also recently looked at other ways to slow down or stop aging at a cellular level, while yet another team is looking into a new class of drugs called senolytics that could help slow aging.
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The new findings challenge one of the current popular theories of aging, that lays the blame for humans’ inevitable downhill slide with mutations that accumulate in our mitochondrial DNA over time. Mitochondrion are sometimes likened to a cellular “furnace” that produces energy through cellular respiration. Damage to the mitochondrial DNA results in changes or mutations in the DNA sequence that build up and are associated with familiar signs of aging like hair loss, osteoporosis and, of course, reduced lifespan.
So goes the theory, at least. But the Tsukuba researchers suggest that something else may be going on within our cells. Their research indicates that the issue may not be that mitochondrial DNA become damaged, but rather that genes get turned “off” or “on” over time. Most intriguing, the team led by Professor Jun-Ichi Hayashi was able to flip the switches on a few genes back to their youthful position, effectively reversing the aging process.
The researchers came to this conclusion by comparing the function level of the mitochondria in fibroblast cell lines from children under 12 years of age to those of elderly people between 80 and 97. As expected, the older cells had reduced cellular respiration, but the older cells did not show more DNA damage than those from children. This discovery led the team to propose that the reduced cellular function is tied to epigenetic regulation, changes that alter the physical structure of DNA without affecting the DNA sequence itself, causing genes to be turned on or off. Unlike mutations that damage that sequence, as in the other, aforementioned theory of aging, epigenetic changes could possibly be reversed by genetically reprogramming cells to an embryonic stem cell-like state, effectively turning back the clock on aging.
For a broad comparison, imagine that a power surge hits your home’s electrical system. If not properly wired, irreversible damage or even fire may result. However, imagine another home in which the same surge trips a switch in this home’s circuit breaker box. Simply flipping that breaker back to the “on” position should make it operate as good as new. In essence, the Tsukuba team is proposing that our DNA may not become fried with age as previously thought, but rather simply requires someone to access its genetic breaker box to reverse aging.
To test the theory, the researchers found two genes associated with mitochondrial function and essentially experimented with turning them on or off. In doing so, they were able to create defects or restore cellular respiration. These two genes regulate glycine, an amino acid, production in mitochondria, and in one of the more promising findings, a 97-year-old cell line saw its cellular respiration restored after the addition of glycine for 10 days.
The researchers’ findings were published this month in the journal Scientific Reports.
Whether or not this process could be a potential fountain of youth for humans and not just human fibroblast cell lines still remains to be seen, with much more testing required. However, if the theory holds, glycine supplements could one day become a powerful tool for life extension.
Similar research from the Salk Institute has also recently looked at other ways to slow down or stop aging at a cellular level, while yet another team is looking into a new class of drugs called senolytics that could help slow aging.
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