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Scientists reverse ageing in mammals and predict human trials within 10 years.

Stashed in: Awesome, Medical Breakthroughs, DNA, DNA

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Early but promising:

Scientists have known for some time that the four genes, which are known collectively as the Yamanaka factors, could turn adult cells back to their stem cell state, where they can grow into any part of the body.

But it was always feared that allowing that to happen could damage organs made from the cells, and even trigger cancer.

However, it was discovered that stimulating the genes intermittently reversed ageing, without causing any damaging side effects.

In mice with a premature ageing disease, the treatment countered signs of ageing and increased their lifespan by 30 per cent. If it worked similarly in humans it could allow people to live until more than 100 years old. In healthy mice it also helped damaged organs to heal faster.

Top Reddit comment:

I am a biogerontologist.

I read the paper.

The research is good. The media's hype is not (of course).

They used mice that already had a premature aging disease, and showed that by intermittently activating the Yamanaka reprogramming factors they could get amelioration of the progeroid phenotypes of the disease. They showed that this also worked in human cells.

The lifespan extension they got was 30%, which means the mice were still shorter-lived than wild type mice.

It was also worth noting that they got some median lifespan extension in their transgenic mice without administering their drug, which means that some of the lifespan extension they saw could have come from genetic background effects after their cross (they had to cross the disease model mice to the inducible construct mice).

So, not bullshit, very intriguing and impressive research, but hardly a "cure for aging".

I particularly like that it lends strong support to the role of epigenetic dysregulation as a fundamental driver of the aging process in post-mitotic tissues.


The underlying cellular processes that drive aging are not fully understood. Various competing hypotheses exist, including telomere erosion, oxidative damage, dna damage accumulation, and the buildup of nondegradable protein aggregates to name a few.

I've always been of the opinion that there is random drift in the elements that control gene expression (epigenetics) in non-dividing cells, and this gradually makes them lose functionality.

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