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obeygiant

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Jan 14, 2002
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To protect the body, aged cells undergo the ultimate sacrifice: they switch on molecular machinery that results in their own death—a process beautifully named “apoptosis,” meaning the “gentle falling of leaves” in ancient Greek.

But sometimes aged cells go rogue. Rather than committing suicide, these cells lurk in our hearts, livers, kidneys and brains, where they silently promote disease. Scientists have long suspected that these “senescent” cells cause us to age, but getting rid of them without harming normal, healthy cells has been challenging.

Now, a collaborative effort between the Erasmus University in the Netherlands and the Buck Institute for Research on Aging in California may have a solution. Published in the prestigious journal Cell, the team developed a chemical torpedo that, after injecting into mice, zooms to senescent cells and puts them out of their misery, while leaving healthy cells alone.

“This is the first time that somebody has shown that you can get rid of senescent cells without having any obvious side effects,” says Dr. Francis Rodeir at the University of Montreal in Canada, who was not involved in the study.

When treated with the drug, aged mice regrew their scraggly fur into luscious coats and saw improved liver and kidney functions. They also seemed more energized, opting to spend their time on a running wheel instead of sleeping in a corner.

Rather than a synthetic chemical, the drug is a small peptide made up of amino acids, the building blocks of protein. Similar peptide drugs are already revolutionizing stroke therapy, and the team plans to begin human safety trials with their anti-aging drug soon.

The study offers the first glimmer of hope that deleting senescent cells could be feasible in people. “It’s definitely a landmark advance in the field,” says Rodeir.​



Last year, scientists at the Mayo Clinic in Minnesota genetically modified mice so that their bodies automatically killed off about 50-70 percent of their senescent cells. After six months of treatment, the mice had healthier kidneys, stronger hearts, and—the most jaw-dropping result—they also lived 20 percent longer than the controls.

Even the scientists were shocked, remarking that they didn’t expect such a dramatic improvement. The study galvanized the field: senescent cells do in fact contribute to aging. And if they can be stopped, maybe we can also slow down the aging clock.

The billion-dollar question was how to make it work in humans, without resorting to gene therapy.​

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will never be made available.

In reality it will be blocked by every pharmaceutical company as will impact their drug sales.
 
will never be made available.

In reality it will be blocked by every pharmaceutical company as will impact their drug sales.

Hogwash. 1) most drugs have ZERO to do with aging and so longer lifespan means greater not lesser profit. 2) better believe someone will want to make a profit selling anti aging drugs. 3) even evil overlords (eye roll) want to live longer.

This will be out faster than viagra
 
it will be for the elite only who can afford it.

If it stops the dead/dying cells causing issue then we live longer and healthier.
They cannot have that now.

Not with the UN agenda 21
 
Seeing as the vast majority of techniques used on mice never end up being applicable to humans, this kind of journalism is exciting in the academic sense only.


That and pumping up the stock price of whoever is funding the research...
 
I'm not sure if big pharma would go for anti-aging drugs. I think the bigger issue would be the ethical debate around it. It would probably boil down to insurance reimbursement (aka profitability), who would probably not cover it. Again, assuming it passes the ethical test.

But all assumes that this technology is transferable to humans. Oftentimes what occurs in animal models is very different than what happens in humans. A rat's lifespan is only a couple years, so the effects on a human could be very different. Peptide drugs also tend to risk immune reactions in humans and nearly always must be injected (impractical).
 
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To protect the body, aged cells undergo the ultimate sacrifice: they switch on molecular machinery that results in their own death—a process beautifully named “apoptosis,” meaning the “gentle falling of leaves” in ancient Greek.

But sometimes aged cells go rogue. Rather than committing suicide, these cells lurk in our hearts, livers, kidneys and brains, where they silently promote disease. Scientists have long suspected that these “senescent” cells cause us to age, but getting rid of them without harming normal, healthy cells has been challenging.

Now, a collaborative effort between the Erasmus University in the Netherlands and the Buck Institute for Research on Aging in California may have a solution. Published in the prestigious journal Cell, the team developed a chemical torpedo that, after injecting into mice, zooms to senescent cells and puts them out of their misery, while leaving healthy cells alone.

“This is the first time that somebody has shown that you can get rid of senescent cells without having any obvious side effects,” says Dr. Francis Rodeir at the University of Montreal in Canada, who was not involved in the study.

When treated with the drug, aged mice regrew their scraggly fur into luscious coats and saw improved liver and kidney functions. They also seemed more energized, opting to spend their time on a running wheel instead of sleeping in a corner.

Rather than a synthetic chemical, the drug is a small peptide made up of amino acids, the building blocks of protein. Similar peptide drugs are already revolutionizing stroke therapy, and the team plans to begin human safety trials with their anti-aging drug soon.

The study offers the first glimmer of hope that deleting senescent cells could be feasible in people. “It’s definitely a landmark advance in the field,” says Rodeir.​



Last year, scientists at the Mayo Clinic in Minnesota genetically modified mice so that their bodies automatically killed off about 50-70 percent of their senescent cells. After six months of treatment, the mice had healthier kidneys, stronger hearts, and—the most jaw-dropping result—they also lived 20 percent longer than the controls.

Even the scientists were shocked, remarking that they didn’t expect such a dramatic improvement. The study galvanized the field: senescent cells do in fact contribute to aging. And if they can be stopped, maybe we can also slow down the aging clock.

The billion-dollar question was how to make it work in humans, without resorting to gene therapy.​

Sign me up!
[doublepost=1493475668][/doublepost]by the time this is on the market...most of the readers of this post will be in the grave yard.
 
With treatments at such an early stage, guesses as to when they might arrive or how far they will stretch human longevity can only be that. Many researchers refuse to speculate. But Kirkland says the informal ambition in his field is to increase healthspan by two to three years in the next decade or more. (The EU has an official goal of adding two years to healthspan by 2020). Beyond that, what effects these drugs might have on extending our healthy lives is even harder to predict. A recent report by UK Human Longevity Panel, a body of scientists convened by insurer Legal and General, based on interviews with leading figures in the field, said: “There was disagreement about how far the maximum lifespan could increase, with some experts believing that there was a maximum threshold that could not be stretched much more than the current 120 years or so, and others believing that there was no limit.”

Nir Barzilai, director of the Institute for Ageing Research at the Albert Einstein College of Medicine, is one of the pessimists. “Based on the biology that we know today, somewhere between 100 and 120 there is a roof in play and I challenge if we can get beyond it.” Venter is one of the optimists. “I don’t see any absolute biological limit on human age,” he says, arguing that cellular immortality – in effect running the clock backwards – should be possible. “We can expect biological processes to eventually get rid of years. Whether this will happen this century or not, I can’t tell you”. Such ideas are just speculation for now. But John Troyer, who studies death and technology at the Centre for Death and Society at the University of Bath, says we need to take them seriously. “You want to think about it now before you are in the middle of an enormous mess.”

What happens if we all live to 100, 110, 120 or beyond? Society will start to look very different. “People working and living longer might make it more difficult for a new generation to get into the labour force or find houses,” says Troyer. And, with ageing delayed, how many children are we talking about as being a normal family? “There is a very strong likelihood there would be an impact on things like family structures.” A 2003 American president’s Council on Bioethics report looked at some of these issues suggesting there may be repercussions for individual psychology, too.

One of the “virtues of mortality” it pointed out is that it may instill a desire to make each day count. Would knowing you had longer to live decrease your willingness to make the most of life? De Grey acknowledges potential practical challenges but cheerily says society would adapt, for example by having fewer children, and with people able to decide when to end their lives. There are pressing questions too about who would benefit if and when these interventions become available. Will it just be the super rich or will market incentives – who wouldn’t want it? – push costs down and make treatment affordable?
Guardian article from 2015
 
I have no idea if this is feasible in humans, but the implications of it are pretty staggering. Healthier people - great! People living longer with no reduction in the birth rate - population growth spiralling out of control.
 
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