Category Archives: aging / life extension

Breaking the age barrier

antiagingpills

Wonder pills for the middle-aged and other medical advances are extending healthy life as never before. Even people in their nineties can benefit. Sarah-Kate Templeton reports

When Dorothy Newcombe fell ill with heart disease at the age of 92, her family thought she had reached the end of her natural lifespan. One of her seven grandchildren and one of her seven great-grandchildren travelled from New Zealand to say goodbye.

After a new treatment particularly targeted at the elderly, Dorothy is still going strong. She goes shopping with her 94-year-old husband, George, does the housework and is back playing bingo at the local church hall. Dorothy, from Liver-pool, has even managed to dance a few steps of a waltz again.

For any nonagenarian to have a new heart valve is remarkable; what makes Dorothy’s case even more special is that she received one in a procedure that allowed her to walk out of hospital just three days after surgery last October.

Last week she said: “Before the operation I wasn’t at all well. I couldn’t walk, I couldn’t bend down. This operation has given me a new lease of life. It has given me a new chance. We can still put on records and have a dance in the house.”

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Slowing Our Aging Clock -World’s Leading Expert Tells How

Just Say NO To Old Age: Professor X isn’t the only one with incredible mental powers: recent research says that you might be even better at brain-boosting, helping heal yourself with the power of a positive attitude – while he can’t even summon up the mental energy to stand.

The power of positive thinking might make us sound infinity percent more likely to wear hemp and say “man” an inappropriate number of times for science reporters (i.e. ever), but it’s real research at Harvard. Professor Ellen Langer has conducted several studies into “mindfulness theory”, researching just how much your attitude affects your actual body. The answer: quite a bit.

One of Benjamin Button’s many stories-within-stories in F. Scott Fitzgerald’s short story, The Curious Case of Benjamin Button, involves the tale of a clock built for the New Orleans train station that is designed to run backwards, in the hope that it will resurrect the First World War dead.

With a similar result in mind, in one experiment Langer shut several septuagenarians in a hotel that had been redecorated in mid-eighties style, eliminating all evidence of the last two decades. Subjects were instructed to act as if they’d really gone all Doctor Who, and after only seven days they were faster, stronger, better than before. Stronger for seventy-year olds, anyway, and certainly stronger than a control group who didn’t get this amateur time-travel and were basically left to think about how damn old they were.

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Also see this article.

Body repair ‘could be ramped up’

A combination of drugs could trick the body into sending its repair mechanisms into overdrive, say scientists.

The technique could be used to speed the healing of heart or bone damage, they claim.

The bone marrow of treated mice released 100 times as many stem cells – which help to regenerate tissue.

Imperial College London scientists reported their work in the journal Cell Stem Cell, but said human trials were some years away.

The release of stem cells by the bone marrow is a natural part of the repair process – different types are sent to replenish tissue depending on the nature of the injury.

However, in some cases, for example the damage caused by heart disease, the repair is not entirely successful, and loss of function persists.

The theory behind the Imperial College research is to boost the quantity of stem cells released, which will hopefully mean a swifter and more complete recovery.

Techniques already exist to increase the numbers of blood cell producing stem cells from the bone marrow, but the study focuses on two other types – endothelial, which produce the cells which make up our blood vessels, and mesenchymal, which can become bone or cartilage cells.

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Harvard Team Unlocks Clues to Genes that Control Longevity

Harvard Medical School Researchers have used a single compound to increase the lifespan of obese mice, and found that the drug reversed nearly all of the changes in gene expression patterns found in mice on high calorie diets–some of which are associated with diabetes, heart disease, and other significant diseases related to obesity.

The research, led by investigators at Harvard Medical School and the National Institute on Aging, is the first time that the small molecule resveratrol has been shown to offer survival benefits in a mammal.

“Mice are much closer evolutionarily to humans than any previous model organism treated by this molecule, which offers hope that similar impacts might be seen in humans without negative side-effects,” says co-senior author David Sinclair, HMS associate professor of pathology, and co-director of the Paul F. Glenn Labs for the Biological Mechanisms of Aging.

“After six months, resveratrol essentially prevented most of the negative effects of the high calorie diet in mice,” said Rafael de Cabo, Ph.D., the study’s other co-senior investigator from the National Institute on Aging’s Laboratory of Experimental Gerontology, Aging, Metabolism, and Nutrition Unit. “There is a lot of work ahead that will help us better understand resveratrol’s roles and the best applications for it.”

Resveratrol is found in red wines and produced by a variety of plants when put under stress. It was first discovered to have an anti-aging properties by Sinclair, other HMS researchers, and their colleagues in 2003 and reported in Nature. The 2003 study showed that yeast treated with resveratrol lived 60 percent longer. Since 2003, resveratrol has been shown to extend the lifespan of worms and flies by nearly 30 percent, and fish by almost 60 percent. It has also been shown to protect against Huntington’s disease in two different animal models (worms and mice).

“The “healthspan” benefits we saw in the obese mice treated with resveratrol, such as increased insulin sensitivity, decreased glucose levels, healthier heart and liver tissues, are positive clinical indicators and may mean we can stave off in humans age-related diseases such as type 2 diabetes, heart disease, and cancer, but only time and more research will tell,” says Sinclair, who is also a co-founder of Sirtris, a company with an author on this paper and which is currently in a phase 1b trial in humans with diabetes using an enhanced, proprietary formulation of resveratrol. [Harvard has license and equity interests with Sirtris, which is not a public company.]

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Harvard Scientists Unravel The Secret Of Aging

As we get older, our health becomes our worst enemy. What’s the secret of living a longer healthy life, is a question still unanswered. At least until today, when Harvard researchers sustain that they might know the secret of aging.

Their paper published in this week issue of the journal Cell is the latest to draw attention to sirtuins, proteins involved in the aging process. Sirtuins become increasingly important as people age, according to lead author David A. Sinclair, a Harvard Medical School professor and co-founder of the Cambridge biotechnology company Sirtris Pharmaceuticals, Inc. The proteins help maintain a youthful pattern of gene expression by ensuring that the genes that should be “off” remain silent.

The same proteins appear to also repair DNA damage as we age, Harvard researchers found.

“The critical protein controls both which genes are off and on as well as DNA repair; it’s used for both processes, and that’s the catch,” said Sinclair.

As we get older, more and more chromosomes get damaged and the SIR1 proteins can’t handle both jobs as well. This causes gene activity to go “haywire” leading to symptoms associated with the process of aging.

Bu the good part is just starting. The scientists have found evidence that the aging process can be slowed. They discovered that mice with more SIRT1 proteins have an improved ability to repair the DNA and to prevent the unwanted changes in the gene expressions.

Previous studies have shown that resveratrol, a chemical found primarily in red wine, helps activate the SIRT1 protein, which aids in the repair of broken chromosome. It’s true that the studies have been conducted on mice, but it’s an important step forward and a reason to believe that the possibility of improving our life is closer than we think.

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Has universal ageing mechanism been found?

An overworked protein that causes yeast to age when it neglects one of its functions may trigger ageing in mice too. If the same effect is found in people, it may suggest new ways to halt or reverse age-related disease.

As we get older, genes can start to be expressed in the wrong body tissues – a process that is thought to contribute to diseases like diabetes and Alzheimer’s. But while sunlight or chemicals are known to cause limited DNA damage, how more widespread changes in gene expression come about has been unclear.

To investigate, David Sinclair and colleagues at Harvard Medical School turned to yeast cells. These produce a dual-function protein called Sir2 that, while being involved in DNA repair, also helps keep certain genes switched off.

As yeast cells age, the protein can’t do both jobs and neglects its role as a gene suppressor.

Now Sinclair’s team has shown that SIRT1, the mammalian version of Sir2, also begins to neglect its gene-suppressor role in mice whose DNA is damaged, and that this may contribute to ageing.

This raises the hope that, if gene-suppressing proteins become similarly overworked in ageing people, they could become prime targets for drugs to keep us young.

This possibility is boosted by the team’s finding that mice engineered to over-express the gene for SIRT1 were better at repairing DNA, more resistant to cancer, and maintained a more youthful pattern of gene expression.

“The most exciting thing is that this work may unify in a single molecular pathway what we know about ageing in different organisms such as yeast and mammals,” says Maria Blasco of the Spanish National Cancer Research Centre in Madrid, who works on mechanisms of cellular ageing.

“It opens up the possibility of restoring youth in the elderly by re-establishing a useful pattern of gene expression,” adds Sinclair.

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Scientists take a step closer to an elixir of youth

Researchers believe boosting the amount of a naturally forming enzyme in the body could prevent cells dying and so lead to extended, healthier, lifespans.

The protein telomerase helps maintain the protective caps at the ends of chromosomes which act like the ends of shoelaces and stop them unravelling.

As we age, and our cells divide, these caps become frayed and shorter and eventually are so damaged that the cell dies. Scientists believe boosting our natural levels of telomerase could rejuvenate them.

A team at the Spanish National Cancer Centre in Madrid tested the theory on mice and found that those genetically engineered to produce 10 times the normal levels of telomerase lived 50 per cent longer than normal.

Maria Blasco, who led the research, told the New Scientist said that the enzyme was capable of turning “a normal, mortal cell into an immortal cell”.

She added that she was optimistic that a similar approach may eventually lead to extended human lifespans – though she urged caution.

“You can delay the ageing of mice and increase their lifespan,” she said.

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Elderly dogs to be offered genetic enhancement to make them young again

An American professor is preparing to market a form of canine gene therapy, which would see dogs injected with substances which switch off the genes that regulate their muscle growth.

Prof Lee Sweeney, from the University of Pennsylvania, has pioneered research into gene transfer technology, a field in which poorly functioning and abnormal genes are manipulated, switched off or replaced.

Ten years ago he created “mighty mice” in the lab with enormous muscles and strength in old age. Now he says experiments on dogs have been so successful that he is preparing to market the treatments to owners of ageing pets across the United States.

He said: “We are now in the final stages of getting all the approvals to offer this through the veterinary hospital as a treatment to try to improve strength in pet dogs.

“As the dogs get weak their owners get upset that they can’t walk around any more. So we’re hoping that within the next year we will begin the era of genetic enhancement in dogs.”

Under the therapy, dogs would be given an injection into the liver of an inhibitor which switches off the gene which produces myostatin, a protein which inhibits muscle growth in animals and humans.

The treatment has passed laboratory trials, but regulatory authorities are now discussing whether the dogs would have to be held in quarantine after treatment, because of possible risks if humans came into contact with their waste after the procedure, Prof Sweeney said.

Scientists hope the same technology could be used in humans, to treat serious genetic diseases such as muscular dystrophy.

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Tests start on pill that could lengthen millions of lives

A drug that combines four different medicines and could halve deaths from heart attacks and stroke around the globe will enter human trials this week in London.

The once-a-day polypill has been the dream of doctors for many years, but because the drugs it contains, including aspirin, are cheap, there has been no financial incentive for the pharmaceutical industry to get involved.

Now, however, international teams of researchers, with the backing in the UK of the Wellcome Trust and the British Heart Foundation, are just a few years away from making the polypill an accessible reality.

Difficulties in combining four drugs in one tablet have been overcome and the Red Heart pill, as it has been christened, has been manufactured by the Indian generic drug company Dr Reddy’s. Volunteers are now being recruited for a 12-week pilot trial which will involve up to 700 people in six countries. If all goes well, the main trial with 5,000 to 7,000 volunteers will begin at the end of next year.

Anthony Rodgers, co-director of the clinical trials unit at the University of Auckland, leader of the project, said it had been a struggle to get the polypill this far. “The chances of mainstream pharmaceutical industry taking this on are slim.

“We spent a few years around about 2000-2002 trying to persuade a number of companies to do this, but got nowhere. Basically, their whole business model is around people paying a few hundred pounds a year for the latest blockbuster drug. A pill with established medicines that halved cardiovascular risk and could be available for £20 a year could be seen as a threat.”

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Yeah, let’s keep screwing around with health problems so people can make money off it.

The current greed based economy we have today just doesn’t have the right priorities…

Prevailing Theory of Aging Challenged in Stanford Worm Study

Age may not be rust after all. Specific genetic instructions drive aging in worms, report researchers at the Stanford University School of Medicine. Their discovery contradicts the prevailing theory that aging is a buildup of tissue damage akin to rust, and implies science might eventually halt or even reverse the ravages of age.

“We were really surprised,” said Stuart Kim, PhD, professor of developmental biology and of genetics, who is the senior author of the research.

Kim’s lab examined the regulation of aging in C. elegans, a millimeter-long nematode worm whose simple body and small number of genes make it a useful tool for biologists. The worms age rapidly: their maximum life span is about two weeks.

Comparing young worms to old worms, Kim’s team discovered age-related shifts in levels of three transcription factors, the molecular switches that turn genes on and off. These shifts trigger genetic pathways that transform young worms into geezers. The findings will appear in the July 24 issue of the journal Cell.

The question of what causes aging has spawned competing schools of thought. One side says inborn genetic programs make organisms grow old. This theory has had trouble gaining traction because it implies that aging evolved, that natural selection pushed older organisms down a path of deterioration. However, natural selection works by favoring genes that help organisms produce lots of offspring. After reproduction ends, genes are beyond natural selection’s reach, so scientists argued that aging couldn’t be genetically programmed.

The alternate theory holds that aging is an inevitable consequence of accumulated wear and tear: Toxins, free-radical molecules, DNA-damaging radiation, disease and stress ravage the body to the point it can’t rebound. So far, this theory has dominated aging research.

But the Stanford team’s findings told a different story. “Our data just didn’t fit the current model of damage accumulation, and so we had to consider the alternative model of developmental drift,” Kim said.

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