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scrapper t1_j7d7fzc wrote

Surely this gene slows aging effect rather than rewinding them?


Nyrin t1_j7dbuv8 wrote

Sometimes. "Aging" is a remarkably complex set of processes and still in its very early stages of being properly understood. Some causes of aging, when treated and addressed, really do "reverse" apparent age — in reality, this is addressing flaws in replication process and moving that function back towards normal, but from the outside it does appear that the new tissue is functionally "younger" than the old.

One special case (telomerase deficiency) induced and exercised in mice:

Everything in your body (almost) is continuously replacing itself at various speeds. If there's a problem that's causing replicated cells to behave as if they're more degraded ("older") than they otherwise would be, then treating that and having the next replacement round be more functional than its precessor is effectively "reducing age" as an apparent and functional measure.

If the source cells have accumulated replication errors or otherwise been intrinsically "damaged," however, you need much more intensive and hitherto "exotic" treatments to make all the trillions of pieces of "future human" to look and act younger than "current human," and "slowing aging" is a lot more readily attainable in those circumstances.


SerialStateLineXer t1_j7e4iax wrote

> The Bristol team, led by Professor Paolo Madeddu, has found that a single administration of the mutant anti-aging gene halted the decay of heart function in middle-age mice. Even more remarkably, when given to elderly mice, whose hearts exhibit the same alterations observed in elderly patients, the gene rewound the heart’s biological clock age by the human equivalent of more than ten years.

That's where "rewind" comes from. It restored cardiac function in elderly mice when administered late in life.