[Twendypreency]

no followup?

[asypecresty]

no followup?

I don't disagree. In fact, the article itself urged the same caution you did and for more or less the same reason. They were just a bit more "calm" about it.

It may be a premature choice of phrase. Before speculation on human applications can even begin, the researchers need to determine whether telomerase activation works for “normal” mice, and not just a single strain genetically engineered to age prematurely.

But its all step by step, and still promising. Slow and steady wins the race.

[medio]

Gnius, I would suspect the news is the reversal affect - as you say, the aging affect has been known for a long time.

However, sign me up for the human trials...

[asypecresty]

http://www.wired.com/wiredscience/20...edium=facebook

By tweaking enzymes that prevent chromosome tips from unraveling, researchers have shown age-related tissue degeneration can be reversed in some mice.

Medical breakthroughs involving mice must be taken with rock-sized grains of salt because, despite their genetic similarity, the rodents aren’t humans. The latest findings, published online by the journal Nature on November 28, are no exception. Nevertheless, they provide the first compelling evidence of aging’s reversal — not just delay — in a high-level organism.

The work represents an “unprecedented reversal of age-related decline in the central nervous system and other organs vital to adult mammalian health,” wrote the team led by Ronald DePinho, a cancer geneticist at Harvard Medical School.

The researchers genetically engineered mice to lack telomerase, the key enzyme ingredient in structures called telomeres that cap the tips of chromosomes and prevent them from fraying.

In healthy mammals, telomeres shorten slightly with each round of cell division and such shortening is linked to a variety of age-related disorders.
DePinho’s telomerase-less mice tended to be prematurely aged and infertile with small brains, damaged intestines and poor senses of smell.

Four weeks after the researchers gave them a drug designed to stimulate telomerase production, however, these visible signs of aging had reversed.

In a press release, DePinho described the transformation as “akin to a Ponce de León effect,” referring to the 16th century conquistador’s search for a fountain of youth.

It may be a premature choice of phrase. Before speculation on human applications can even begin, the researchers need to determine whether telomerase activation works for “normal” mice, and not just a single strain genetically engineered to age prematurely.

Such strain-dependent effects have confounded the promise of drugs designed to mimic the apparent longevity-extending effects of low-calorie diets. But even if the findings are never translated directly to humans, they may still provide insight into the physiological basis of aging itself — something that, despite centuries of study, has yet to be pinned down.

[ftqwhbvxlcfop]

despite their genetic similarity, the rodents aren’t humans.

Wow, seriously?

[Twendypreency]

The researchers genetically engineered mice to lack telomerase, the key enzyme ingredient in structures called telomeres that cap the tips of chromosomes and prevent them from fraying.

DePinho’s telomerase-less mice tended to be prematurely aged and infertile with small brains, damaged intestines and poor senses of smell.

Four weeks after the researchers gave them a drug designed to stimulate telomerase production, however, these visible signs of aging had reversed.

So if you delete a gene that's necessary to maintain proper life and development, you get trouble. And when you turn it back on, you can fix the trouble you've created... genius.

It's an important work, but it's so far from the sweeping generalizations it implies, that's it's not even funny. Nor is this truly news, since the link between telomeres and aging has been described since....

Telomeres shorten during ageing of human fibroblasts.
Harley CB, Futcher AB, Greider CW.
Nature. 1990 May 31;345(6274):458-60.

It's pretty well understood at this point, that telomeres aren't the complete answer (if at all), largely through studies in mice, since mouse cells have MUCH longer telomeres than humans do, and in-vivo mouse telomeres pretty much never shorten enough to affect coding sequences of chromosomes before the death of the animal.

The fundamental problem with the Wired interpretation (and I imagine it's a fairly conservative one, and other news channels will run news stories about: AGING=SOLVED...

Just imagine - if someone breaks your jaw, a maxillofacial surgeon will put pins in it to put it back together, and it will work better than when it was broken. Does that mean that if you put pins in a healthy jaw it will work better?

[asypecresty]

So if you delete a gene that's necessary to maintain proper life and development, you get trouble. And when you turn it back on, you can fix the trouble you've created... genius.

It's an important work, but it's so far from the sweeping generalizations it implies, that's it's not even funny.

Do you understand the fundamental problem with this approach?

Just imagine - if someone breaks your jaw, a maxillofacial surgeon will put pins in it to put it back together, and it will work better than when it was broken. Does that mean that if you put pins in a healthy jaw it will work better?

I think they were trying to prove a correlation and then work from there. Are you completely denying the validity of the experiment, or simply pointing out some caveats?

(Which I am going to suspect the researchers are probably smart enough to be aware of)

[Twendypreency]

I think they were trying to prove a correlation and then work from there. Are you completely denying the validity of the experiment, or simply pointing out some caveats?

(Which I am going to suspect the researchers are probably smart enough to be aware of)

^ I wrote more about this above, please read it. Especially the part about the mouse experiments.

P.S. I think I'm more than qualified to criticize the paper if I see fit. Since I haven't yet read the original, I will withhold much of my criticism for the moment. I'll read it and report back.

[Twendypreency]

Ok... read it...

So basically the key points of the paper are:
1. it took the authors 4 generations of TERT-/- homozygous mice to achieve notable damage due to telomere shortening
2. the DNA damage response and activation of cell death cascade can be not just curbed, but reversed in cells, if TERT is expressed in TERT -/- cells that have undergone DNA damage
3. some organ function can be restored to rapidly-dividing tissues damaged by telomere shortening, after 4 weeks of TERT expression.

Interesting... largely because they are showing some reversal of the DNA-damage response... which is why the paper is in Nature.

But little impact on aging research, aside from the encouraging thought that perhaps some of the effects of aging can be reversed, if we ever find the triggers (if they are not merely accumulated mutations and the like), as well as a way to fix them.