An end to grey hair and crows-feet could be just 10 years away after scientists showed it is possible to reverse ageing in animals.
Using a new technique which takes adult cells back to their embryonic form, US researchers at the Salk Institute in California, showed it was possible to reverse ageing in mice, allowing the animals to not only look younger, but live for 30 per cent longer.
The technique involves stimulating four genes which are particularly active during development in the womb. It was also found to work to turn the clock back on human skin cells in the lab, making them look and behave younger.
Scientists hope to eventually create a drug which can mimic the effect of the found genes which could be taken to slow down, and even reverse the ageing process. They say it will take around 10 years to get to human trials.
The way BioViva founder Elizabeth Parrish sees it, biological aging is a disease – and she’s willing to bet her life on a cure.
Last fall, the 45-year-old Seattle-area woman underwent an experimental type of gene therapy aimed at addressing some of the big effects of aging, including loss of muscle mass and a shortening of the chromosomes’ telomeres. The procedure was reportedly done in Colombia, to get around U.S. regulations.
The idea of having gene therapy done on yourself raised eyebrows in the biotech community, but Parrish was unfazed.
“I 100 percent believe that it will work, or else I wouldn’t have done it,” Parrish told GeekWire during an interview in February. “I didn’t try to flame out in glory. The research shows that it should absolutely work.”
Now BioViva is reporting that it does seem to work, at least on Parrish’s telomeres. And that’s likely to fuel a debate over the widening scientific quest for greater longevity – conducted not only by BioViva, but by other ventures such as Human Longevity Inc. This week, Human Longevity announced a 10-year deal with AstraZeneca to analyze 500,000 DNA samples for anti-aging clues.
Parrish is already trying to follow up on a couple of clues through Bioviva USA, the privately held company she founded on Bainbridge Island last year. Bioviva announced its own deal this week with a London-based investment fund called Deep Knowledge Life Sciences.
One of BioViva’s anti-aging clues has to do with a protein called myostatin: Research suggests that genetically blocking the production of myostatin could help preserve age-related muscle loss.
The other clue has to do with telomeres, the stretches of DNA at the ends of our chromosomes that are thought to protect our genetic data from harmful mutations – much as the plastic tips on the ends of shoelaces keep them from unraveling. As we age, those telomeres become shorter, and the protective effect is gradually lost.
The gene therapy that Parrish underwent was aimed at inhibiting myostatin and building up telomeres.
At the gene-editing summit, you can’t miss George Church. He’s the big guy with the bushy beard and wavy hair, someone who looks like he stepped out of an 18th century painting of “natural philosophers.” Church, who is 61, is among several hundred scientists, policymakers and thinkers on hand to discuss the powerful technology known as CRISPR, a new method for editing genes. The technique was invented in the past four years, and Church is among those who can claim at least partial credit for the innovation (there’s an intense legal battle over patents — a story for another day).
I mentioned to Church that this is the kind of work for which Nobels are awarded. He quickly responded that there are more important things in the balance than prizes. There are cures for human diseases, he said.
Church thinks that one of the ailments he can cure is aging. When I met him early this year, in his laboratory at Harvard Medical School, where he is professor of genetics, he expressed confidence that in just five or six years he will be able to reverse the aging process in human beings.
“A scenario is, everyone takes gene therapy — not just curing rare diseases like cystic fibrosis, but diseases that everyone has, like aging,” he said.
Researchers from the Salk Institute for Biological Studies in California have tested an experimental drug on rapidly-aging mice, with the treatment designed to combat aspects of aging closely associated with Alzheimer's. The results were very positive, with treated mice exhibiting better memory, cognition and more.
Alzheimer's is a widespread and progressive disease that chiefly affects the elderly. There are currently more than five million people with the condition in the United States alone.
The Salk research is looking to tackle the disease from a new angle. It expands upon a previous study conducted back in 2013, working with a potent memory-enhancing and neurotrophic drug called J147. Unlike most medicines designed to combat the disease, J147 was synthesized after looking at age-associated brain toxicities, and looks to tackle the major risk factor for the disease – old age itself.
The older research looked at the effect of J147 on mice with an inherited form of Alzheimer's, finding that it was able to prevent and even reverse memory loss in subjects. While that was promising, inherited Alzheimer's is far less common than cases of the disease triggered by old age.
The new study looked to discover whether the experimental drug is as effective at fighting Alzheimer's caused by old age, which is responsible for 99 percent of cases. Once the results were in, things were looking very positive, with the researchers surprised by how effective it had proved.
"We did not predict we'd see this sort of anti-aging effect," says lead author Antonio Currais. "But J147 made old mice look like they were young, based upon a number of physiological parameters."
Doctors and scientists want drug regulators and research funding agencies to consider medicines that delay ageing-related disease as legitimate drugs. Such treatments have a physiological basis, researchers say, and could extend a person’s healthy years by slowing down the processes that underlie common diseases of ageing — making them worthy of government approval. On 24 June, researchers will meet with regulators from the US Food and Drug Administration (FDA) to make the case for a clinical trial designed to show the validity of the approach.
Current treatments for diseases related to ageing “just exchange one disease for another”, says physician Nir Barzilai of the Albert Einstein College of Medicine in New York. That is because people treated for one age-related disease often go on to die from another relatively soon thereafter. “What we want to show is that if we delay ageing, that’s the best way to delay disease.”
Barzilai and other researchers plan to test that notion in a clinical trial called Targeting Aging with Metformin, or TAME. They will give the drug metformin to thousands of people who already have one or two of three conditions — cancer, heart disease or cognitive impairment — or are at risk of them. People with type 2 diabetes cannot be enrolled because metformin is already used to treat that disease. The participants will then be monitored to see whether the medication forestalls the illnesses they do not already have, as well as diabetes and death.
On 24 June, researchers will try to convince FDA officials that if the trial succeeds, they will have proved that a drug can delay ageing. That would set a precedent that ageing is a disorder that can be treated with medicines, and perhaps spur progress and funding for ageing research.
During a meeting on 27 May at the US National Institute on Aging (NIA) in Bethesda, Maryland, Robert Temple, deputy director for clinical science at the FDA’s Center for Drug Evaluation and Research, indicated that the agency is open to the idea.
Age-associated accumulation of somatic mutations in mitochondrial DNA (mtDNA) has been proposed to be responsible for the age-associated mitochondrial respiration defects found in elderly human subjects. We carried out reprogramming of human fibroblast lines derived from elderly subjects by generating their induced pluripotent stem cells (iPSCs), and examined another possibility, namely that these aging phenotypes are controlled not by mutations but by epigenetic regulation. Here, we show that reprogramming of elderly fibroblasts restores age-associated mitochondrial respiration defects, indicating that these aging phenotypes are reversible and are similar to differentiation phenotypes in that both are controlled by epigenetic regulation, not by mutations in either the nuclear or the mitochondrial genome. Microarray screening revealed that epigenetic downregulation of the nuclear-coded GCAT gene, which is involved in glycine production in mitochondria, is partly responsible for these aging phenotypes. Treatment of elderly fibroblasts with glycine effectively prevented the expression of these aging phenotypes.
Researchers at the Stanford University School of Medicine have developed a new procedure to increase the length of human telomeres. This increases the number of times cells are able to divide, essentially making the cells many years younger. This not only has useful applications for laboratory work, but may point the way to treating various age-related disorders – or even muscular dystrophy.
Telomeres are the caps at the ends of our chromosomes that protect the DNA code of the genome. Linked to aging and disease, they are 8,000 to 10,000 nucleotides long in young people, but this decreases as we age (a nucleotide is an organic molecule that is a subunit of nucleic acids DNA and RNA). The researchers have found a way to lengthen a telomere by 1,000 nucleotides, which Dr. Helen Brau, professor of microbiology and immunology at Stanford, says is the equivalent of "many years of human life."
Telomeres shorten each time a cell divides and at a certain point, when they reach a critical length, the cell can no longer divide and will die. Their limited lifespan means that growing cells in laboratories can be tricky, given there can only be so many cell doublings before they give up the ghost. Telomere function in humans has been linked to many diseases and they have been studied for decades, often in the hope of better understanding or delaying the aging process.
Cells treated with Stanford’s procedure multiply in a similar way to much younger cells, compared with untreated cells of the same age. According to the researchers, skin cells with telomeres lengthened by the procedure were able to divide around 28 more times than untreated cells, while muscle cells divided about three more times. With this new procedure, which uses modified RNA, many more cells can be easily generated for study and drug development or disease modeling.
In little more than half a century the average Chinese life span has almost doubled. Life expectancy in China is now 76 years, nearly on par with the U.S.’s 79 years. Yet this tremendous boon comes with a dark side: an aging population.
China’s one-child policy throttled population growth so successfully that the proportion of elderly Chinese is now soaring. A 2011 report from the Chinese Academy of Social Sciences predicts that the percentage of the population that is 65 or older will triple between 2000 and 2050. With an aging population comes a greater burden of diseases, chief among them neurodegeneration. Already China has more than nine million people with some form of dementia and more cases of Alzheimer’s disease than any other country, according to a 2013 paper in The Lancet. Its authors dubbed dementia “the single largest challenge to health and social care systems” in China.
The consequences of this trend are profound, and the country has only recently begun to prepare for them. In 2009 the government committed $124 billion to overhauling health care, with a goal of providing basic health insurance for 90 percent of its citizens. The plan also highlighted mental health services as a top priority for the first time. Last year China implemented its first mental health law, which expands psychiatric services throughout the country. Although the policy does not explicitly mention dementia, it underscores the urgent need for community mental health clinics, which could end up aiding families struggling to cope with a relative’s dementia.
To find out more about the implications of China’s demographic shift and the steps the country can take to buffer itself, Scientific American spoke with Michael Phillips, a psychiatrist who has lived in China for 30 years, during the annual meeting of the American Psychiatric Association last week. Phillips has dual appointments at Shanghai Jiao Tong University School of Medicine and the Collaborative Center for Global Mental Health at Emory University.
REGENERATIVE medicine—the idea that it is possible to renew old, worn-out tissue and thus keep a body going beyond the point when its organs start to fail—is an attractive idea. To that end, much effort has been put into creating and nurturing so-called pluripotent stem cells. These, when appropriately nudged, can be induced to turn into cells of any other type. They might thus be used for all sorts of repairs. Pluripotent cells, which once had to be extracted from embryos, can now be made routinely from body cells (skin cells, for example). Experiments are therefore going on to see if, when made from the cells of a particular individual, they might be used to repair damage to that person’s organs without (as a transplant from someone else would) attracting the attention of his immune system.
This approach is promising. It would be even better, though, if rather than having stem cells transplanted into it, a degenerate organ could be persuaded to repair itself. Until now, no one has managed to do this. But Clare Blackburn of Edinburgh University, in Britain, and her colleagues have succeeded. As they report in Development, they have treated, in mice, an organ called the thymus, which is a part of the immune system that runs down in old age. Instead of adding stem cells they have stimulated their animals’ thymuses to make more of a protein called FOXN1. This is a transcription factor (a molecular switch that activates genes), and for the thymus it turns out to be an elixir of life.
Women who have babies naturally in their 40s or 50s tend to live longer than other women. Now, a new study shows their brothers also live longer, but the brothers' wives do not, suggesting the same genes prolong lifespan and female fertility, and may be more important than social and environmental factors.
"If women in your family give birth at older ages, you may well have a chance of living longer than you would otherwise," says the study's lead author, demographer Ken R. Smith, a professor of family and consumer studies at the University of Utah. "If you have a female relative who had children after age 45, then there may be some genetic benefit in your family that will enhance your longevity."
For descendants of the Utah and Quebec pioneers studied, "you may be able to look at the ages when your female ancestors gave birth – rather than just their longevity – in estimating how long you may live," says Smith, whose study will be published online May 4 and in the June 10 print issue of the Journal of Gerontology: Biological Sciences.
The researchers examined high-quality genealogical records from the Utah Population Database at the University of Utah with its records of 1.6 million Utah Mormon pioneers and their descendants. They also used the University of Montreal's Program on Demographic History Research, which has records on 400,000 people who lived in heavily Catholic Quebec between 1608 and 1850.
Specifically, the study involved the records of 11,604 Utah men who were born between 1800 and 1869 and who had at least one sister who lived at least to age 50; and the records of 6,206 Quebec men who lived between 1670 and 1750, and had at least one sister who lived to 50 or older. The key findings:
Women who had "late fertility" – a birth at age 45 or older – were 14 percent to 17 percent less likely to die during any year after age 50 than women who did not deliver a child after age 40. That confirmed earlier studies. But those studies did not determine if the women gave birth later and lived longer because of genes or because of social and environmental factors such as good nutrition or healthy living.
Brothers who had at least three sisters, including at least one sister who gave birth at age 45 or later, were 20 percent to 22 percent less likely to die during any year after age 50 than brothers who had no "late fertile" sisters. That indicates what earlier studies did not, namely, the same genes may influence the lifespan of both sexes and women's ability to give birth at older ages.
The brothers' wives didn't have longer lives, suggesting any environmental or social factors that influence lifespan had only a weak influence, and that genes may explain why brothers lived longer when they had a sister who gave birth in her 40s.
The study didn't address how much longevity is due to genetics, but Smith says scientists believe genes account for up to 25 percent of differences in longevity.
A variation in the gene FOXO3A has a positive effect on the life expectancy of humans, and is found much more often in people living to 100 and beyond – moreover, this appears to be true worldwide. A research group in the Faculty of Medicine at the Christian-Albrechts-University in Kiel (CAU) has now confirmed this assumption by comparing DNA samples taken from 388 German centenarians with those from 731 younger people. The results of the study appear this week in the prestigious American scientific journal Proceedings of the National Academy of Sciences ("PNAS").
Previously, in September 2008, an American research team led by Bradley J. Willcox had published in PNAS a study that indicated a higher frequency of this genetic variation in long-lived Americans of Japanese origin (ages 95 and above). Professor Almut Nebel, the scientific leader of the "Research Group for Healthy Ageing" at Kiel, comments: "That published result is only of scientific value if it can be confirmed in a study with an independently chosen sample population. Without that there must still remain a tinge of doubt. We have now eliminated that uncertainty about the connection between FOXO3A and longevity, both by our results from the German sample study and by the support from our French partners in Paris, whose research on French centenarians showed the same trend. This discovery is of particular importance as there are genetic differences between Japanese and European people. We can now conclude that this gene is probably important as a factor in longevity throughout the world."
FOXO3A is of great interest for genetic research on ageing, since it was reported in the 1990s that the gene was connected with ageing processes in worms and flies. It is because of those observations that the Kiel research group at the Institute of Clinical Molecular Biology has been working for a long time on variations of this gene in humans.
"The most difficult problem is to get enough old people, especially those aged 100 or more, to take part in such a study. Interestingly, the genetic effects are much more evident in 100-year-olds than in 95-year-olds", notes the first author of the report, Dr. Friederike Flachsbart of the Institute of Clinical Molecular Biology at Kiel University.
This is probably the one time in my life I am really happy that gene therapy is still very much a research treatment: ie no Boomers 43v3r. whew.
My wife will be back in 36 hours and I will be very, very happy when that happens. In the mean time, I find myself unable to sleep and decided to watch THEM! again. Quietly, to be sure, since my daughter is fast asleep and that last thing I want is for her to have some ant enduced nightmares especially because of bad child actors.
However since the net is such a useful tool, I decided to browse up some info on the movie. IMDB was a place to start and decided to go through and look up abit on the actors and actresses. There were a few actors there that caught my attention. I didn't realize the hero policeman - a New Mexico State Police Officer (*looks green* just kidding, mostly, but if he'd been border patrol, I'd not be) was also the old and suicidal parolee in The Shawshank Redemption. Wow. Talk about a very long career. Another interesting one was the old professor. My mother loved Miracle on 34th Street and damned if as soon as I read that in his bio that the voice snapped into place. Also there for a blip was a rather younger Spock: man, talk about getting stuck in a genre.
However, the one that struck me more than any was the woman that played Pat, also supposed to be a PhD Dr. It wasn't for anything that she was overly beautiful or whatnot: not bad, not really my taste, but y'know the period costume might have had some neagtive effect. No, what struck me, big time, was that at the time of the film, she was 21. Yep, 21. I'd have guessed a half decade older. Perhaps even pushing 30. Nope. Just 21. Interesting that I took her for that. I thought about the 21 yos I've known, and...I just have to wonder if we're aging a bit differently these days. I mean, the 21 yos these days still look, well, almost like teens, comparatively.
That's not meant as a put down or whatever, just that it's a "Huh! That's odd!" moment.
