A single small molecule can restore muscle strength, promote brain cell growth and reduce inflammation in old mice, according to a new study.
So far, the anti-aging molecule has only been tested on rodents and human cells in a lab dish, but the researchers say the results are compelling enough to allow the compound to be tested in humans, possibly within a few years.
“Given the strength of the preclinical data, it is my view that there is a justification for moving forward with this,” the study’s senior author said. Dr. Ronald DepinhoHe is a professor and former director of the University of Texas MD Anderson Cancer Center.
“We believe this mechanism could have beneficial effects on things that influence healthspan,” DePinho told Live Science, potentially allowing people to live healthier lives into old age.
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Reversing aging with one molecule
A new study published June 21 in the journal Neurology & Neurology says: cellThe researchers aimed to increase the amount of telomerase reverse transcriptase (TERT), a protein that decreases with age.
TERT is a key cog in the cellular machinery that extends cell length. Telomere — Protective caps to prevent fraying of edges ChromosomesTelomere shortening is aging This shortening can also lead to age-related diseases such as cancer. As we age, chemical tags accumulate on our chromosomes, causing them to shorten.EpigeneticSome of these changes turn off the TERT gene, causing cells to make less of the protein.
This threatens telomere integrity and has far-reaching effects on the expression levels of other genes.TERT appears to be a master controller of a set of genes associated with aging, including genes involved in brain cell growth and aging. AgingAs we age, our cells become like zombies, and as the number of zombies increases, they can cause harmful inflammation Inside the body.
“Our lab is the first to demonstrate that aging is a reversible process and that TERT can mediate the reversal of that change,” DePinho said. In 2010Using an experimental technique, DePinho and his colleagues reported that when they turned off the TERT gene in mice, the animals began to age prematurely.
“When we turned it back on, we expected it to just stop aging, but we actually saw it rejuvenate,” Depinho said.
This rejuvenation was seen in cells throughout the body. Subsequent work by the team It has been shown to restore “youthful” levels of TERT in mouse models, Alzheimer’s disease Signs of the disease, such as the buildup of abnormal proteins in the brain, improved.
Given these results, in their new study, the researchers wanted to find a drug-like substance that could boost TERT to levels found in healthy, young cells. They developed a screen using mouse cells engineered to carry the human version of the TERT gene. They screened a total of 653,000 compounds and landed on one that seemed the most potent, which they named TERT activating compound (TAC).
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In a lab dish, the molecule interacts with healthy human cells and Werner syndromea rare condition that causes rapid and premature aging. When exposed to the molecule, these cells experienced significant lengthening of telomeres.
In mice injected with TAC, the molecule boosted TERT in tissues throughout the body, including the brain, DePinho said, indicating the drug can easily travel to the brain, something many molecules cannot do.
The researchers tested TAC in aged mice after short-term treatment (as little as one week) and long-term treatment (six months). Short-term treatment reversed signs of aging in blood cells, reduced known drivers of aging in many tissues, and promoted molecules important for brain cell growth. Long-term treatment promoted brain cell growth. HippocampusIt acts on the brain’s key memory centre, and also appears to improve the performance of rodents in memory tests. Further tests showed that it also improved the coordination and muscle strength of the mice.
TAC works by activating a cascade of events in cells that turns on a master gene regulator and ultimately unmutes the TERT gene. These effects are temporary, peaking about eight hours after injection and fading after 24 hours, DePinho says.
Within that time frame, the drug “restores physiological, youthful levels of TERT,” he said.
More research is needed before TAC can reach human patients. The next steps will be to refine the drug to make it more effective and to identify and eliminate any harmful effects (which weren’t seen in these initial tests). DePinho said the drug, or a derivative of it, will need to undergo further animal testing before moving on to trials in healthy human volunteers and then patients with various age-related diseases.
In theory, the drug could be studied as a way to prevent age-related diseases before they begin, DePinho said, but it would likely first be approved for specific diseases like Alzheimer’s.
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