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We help you stay up to date with the most interesting news in medicine, politics and the healthy life extension community. You can help us by contacting us when you see interesting items online. You can search past news postings through Google by using the form to the right.
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| Regenerative medicine advances, step by step: "researchers have developed an unlimited number of pure insulin-producing cells from mouse embryonic stem cells (ESCs). ... These pure insulin-producing cells, which according to electron microscopy studies, have the same sub-cellular structures as the insulin-producing cells naturally found in the pancreas, were highly effective in treating diabetes in the mouse model. The transplants of pure insulin-producing cells reduced the blood glucose levels of diabetic mice with high blood glucose levels. ... None of the diabetic mice involved in the transplant experiments developed teratoma, which are a type of tumour often associated with ESCs and which could complicate their use in human therapeutic treatment. Furthermore, the pure insulin-producing cells managed to retain their insulin-production and glucose-sensing capacity over time. ... Besides providing a tool to facilitate basic research in test tubes and animals, these insulin-producing cells may be also used to replace the isolated native pancreatic cells that are hard to obtain in a large amount, for pharmacological tests." |
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| From Ouroboros: "In addition the 23 chromosome nuclear genome most of us are familiar with, mitochondria contain their own, distinct genome. Each mitochondrion contains several copies of this genome, and most cell types contain hundreds of mitochondria per cell. ... [Researchers] measured the number of abasic sites [or AP sites] in the mitochondrial genome of young and aged rat brain. AP sites are positions along the DNA backbone where no adenine, guanine, cytosine, or thymine is attached; they are among the most frequent damages to DNA. The authors showed that in normally feeding animals, the number of AP sites increases with age - but calorie restricted (CR) mice did not show such an increase." Since accumulating mitochondrial DNA damage is a root cause of much age-related biochemical damage throughout the body, and since calorie restriction extends healthy longevity in laboratory animals, it makes sense that CR reduces the rate at which this damage accumulates. |
| From EurekAlert!: researchers "have identified for the first time biomarkers of aging which are highly predictive of both chronological and physiological age. Biomarkers are biochemical features that can be used to measure the progress of disease or the effects of treatment. The research involves nematode worms, microarrays which measure changes in gene expression, and complex computer algorithms. This is the first step toward identifying similar biomarkers in humans which would provide a means of scientifically validating anti-aging therapies. ... This is the first evidence that physiological age can be predicted non-subjectively. This is a first step; our results were not perfect, but we were able to predict the ages of the animals 70% of the time, which is far better than anything that has been done before. ... Research into the biology of aging in humans has been hampered by the lack of irrefutable biomarkers that correlate with the aging process. I am confident that at some point there will be a non-subjective method of determining how old someone is with a high level of confidence." |
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| A prodrome is an early set of non-specific symptoms that herald a particular disease. Here, researchers point to chronic inflammation as a prodrome of Alzheimer's (AD): "Recently, the term 'inflammaging' was coined [to] characterize a widely accepted paradigm that ageing is accompanied by a low-grade chronic up-regulation of certain pro-inflammatory responses. Inflammaging differs significantly the from [traditional] acute inflammation in that it is characterized by a relative decline in adaptive immunity ... While the over-active innate immunity characteristic of inflammaging may remain subclinical in many elderly individuals, a portion of individuals (postulated to have a "high responder inflammatory genotype") may shift from a state of "normal" or "subclinical" inflammaging to one or more of a number of age-associated diseases. ... Although conditions of enhanced innate immune response with overproduction of pro-inflammatory proteins are associated with both healthy aging and AD, it is suggested that those who age 'well' demonstrate anti-inflammaging mechanisms and biomarkers that likely counteract the adverse immunity of inflammaging. Thus, opposing the features of inflammaging may prevent or treat the symptoms of AD." |
| From Reuters: "Stem cells from tiny embryos can be used to restore lost hearing and vision in animals, researchers said Tuesday in what they believe is a first step toward helping people. One team repaired hearing in guinea pigs using human bone marrow stem cells, while another grew functioning eyes in tadpoles using frog cells. ... They grew the stem cells into neuron-like cells in lab dishes and then transplanted them into the inner ears of the guinea pigs. Three months later, the animals appeared to have some hearing ... the goal was to regrow the tiny hair cells that are essential for mammals to hear, although she is not sure yet how the stem cells made this happen. They would eventually like to try something similar in humans." These are early stage proof-of-concept demonstrations. It is an illustration of progress that they do not stand out as exceptional amidst advances in the many other lines of regenerative research presently taking place. |
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| I think this post over at Pimm might be an example of the entrepreneurial mind ("why would anyone not want this product that I believe in and toil to build?") being confused by the scientific mind ("look at what can be achieved if we go about it the right way"): "How do you interpret the following situation: we have a life extension technologist whose all endeavors is about pushing this issue to its very limits and making things possible but on the other hand this very life extensionist himself is not driven by actually living as long as he can. It seems that SENS theorist Aubrey de Grey [is] taking roughly the above position [by saying] 'I'm actually not mainly driven by a desire to live a long time. I accept that when I'm even a hundred years old, let alone older, I may have less enthusiasm for life than I have today. Therefore, what drives me is to put myself (with luck) and others (lots and lots of others) in a position to make that choice, rather than having the choice progressively ripped away from me or them by declining health. Whether the choice to live longer is actually made is not.'" I've long said that the purpose of longevity science, like most other scientific progress, is to provide new freedoms and choices - the choice to live longer in good health, and the freedom to do so. |
| Exercise is good for you: "A new study confirms that exercise can reverse the age-related decline in the production of neural stem cells in the hippocampus of the mouse brain, and suggests that this happens because exercise restores a brain chemical which promotes the production and maturation of new stem cells. ... One hypothesis the researchers investigated is that the age-related decline in neurogenesis is tied to a rise in corticosterone in middle age. Elevation of corticosterone has been associated with a drop in the production of new stem cells in the hippocampus. The second hypothesis is that nerve growth factors -- which encourage new neural cell growth but which decrease with age -- account for the drop in neurogenesis. ... production of neural stem cells improved by approximately 200% compared to the middle-aged mice that did not exercise. In addition, the survival of new nerve cells increased by 170% and growth by 190% compared to the sedentary middle-aged mice. ... Based on these results, it appears that nerve growth factor has more to do with these findings than the corticosterone." |
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| From ScienceDaily: "Scientists examined the brains of five deceased people considered super aged because of their high performance on memory tests when they were more than 80 years old and compared them to the brains of elderly, non-demented individuals. Researchers found the super aged brains had many fewer fiber-like tangles than the brains of those who had aged normally. The tangles consist of a protein called tau that accumulates inside brain cells and is thought to eventually kill the cells. Tangles are found in moderate numbers in the brains of elderly and increase substantially in the brains of Alzheimer's disease patients. ... It was always assumed that the accumulation of these tangles is a progressive phenomenon through the aging process. But we are seeing that some individuals are immune to tangle formation and that the presence of these tangles seems to influence cognitive performance." Another type of intracellular aggregate to add to the list for removal by bioremediation. |
| Ouroboros weighs in on a recent demonstration of enhanced longevity via telomerase: "Telomerase is tightly repressed in most somatic cells, and for a very good reason: What do you call a cell with an unlimited division potential that's not a stem cell or germ cell? Usually 'cancer.' ... But what if cancer couldn't form for other reasons? In such a case, we could test the hypothesis that increased regenerative capacity [induced via telomerase] confers increased lifespan. ... why is the effect only on median lifespan? ...Mouse cells have really long telomeres, and telomerase expression is widespread in mouse tissues (though not usually at high enough levels to prevent some telomere shortening at every cell division) ... it makes me wonder what's going on. Could telomerase be doing something else - i.e., something other than lengthening telomeres - that is particularly important in determining median lifespan?" I'd wager on protection of mitochondria, a recently discovered secondary (but possibly more important) action of telomerase. |
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| An article of quotes from various noted aging reseachers: "Aging is caused by the gradual, lifelong accumulation of a wide variety of molecular and cellular damage ... The free radical theory is the most widely accepted theory of aging. But the idea that aging is caused by one thing is naive. One general theory can never fit all. Clearly, it's the combination of genes that your parents dealt you and the lifestyle choices you make and the environmental toxins one is exposed to. One need only count the number of ways a car will fail to start to appreciate that aging can be caused by a large number of problems. Like any machine, it's going to wear out ... about 25 percent of how a person ages is due to inherited genes. Certain genes control a cell's ability to repair damaged DNA. If those genes are defective, they can't do their job. ... Not everybody will be susceptible to diseases like Parkinson's or cancer as they age. But each one of us will lose muscle mass and muscle strength. That's why this research is so important. Frailty affects all of us." |
| From Science News: "the enzyme telomerase can extend the lifespan of mice by about 24 percent. ... Telomerase lengthens telomeres - the 'caps' on the end of chromosomes that protect DNA from damage. Like burning fuses, telomeres normally get shorter each time that most body cells divide. ... While the enzyme enables cells to keep dividing, it also takes cells one step closer to growing and proliferating out of control - that is, becoming cancerous. Lab animals with extra genes for telomerase often die young from tumors. ... [researchers] engineered mice to have not only an extra copy of the gene for telomerase, but also extra anti-tumor genes to combat the enzyme's cancer-causing potential. In the altered mice, signs of aging such as poor coordination or degraded tissue health were delayed compared to mice that had only the extra copies of anti-tumor genes." Most interesting; you might also want to look at recent research that suggests telomerase operates by protecting mitochondria, and less damaged mitochondria means better preservation of telomeres - but, more importantly for life span, less oxidative stress. |
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| From ScienceDaily: "Until now, creating synthetic cartilage was complex but not impossible. The problem was that it was impossible to imitate the perfection of human cartilage due to the difficulty in orienting the collagen nanofibers [in] a particular configuration: in parallel, in a circle, or crossed. The fibers that form the cartilage that protects the knee are aligned in parallel. ... [Researchers have now] achieved this using the electrospinning method. ... collagen nanofibers are obtained by exposing the collagen to electrical discharges. The collagen is extruded, in the form of a nanofiber thread, through a fine needle and is deposited on an electric collector consisting of two grounded plates. The student placed a nonconductive material between the two conducting plates. The nanofibers aligned on top of each other perfectly in parallel lines between the two conducting plates." Innovations in engineering the simpler forms of human tissue have been arriving more rapidly of late - more scientists are involved, the tools are improving, and the cost of research is falling. This is all groundwork for the next decade and tissue engineering of complex replacement organs. |
| Discovering a stem cell population is the first step to regenerating the tissue they support: "A novel protein marker has been found that identifies rare adult liver stem cells, whose ability to regenerate injured liver tissue has the potential for cell-replacement therapy. ... In the future, this marker will allow for the isolation and expansion of these stem cells, which could then be used to help patients whose livers can no longer repair their own tissue. ... In a healthy liver, proliferation of mature liver and bile-duct lining cells is sufficient to maintain the necessary size and function of the organ. This even works when the liver is confronted with mild and acute injury, but the situation changes when injury to the liver is chronic and severe ... For chronic injury, the liver uses a back-up system that stimulates stem cells to proliferate and eventually differentiate into new liver cells. [Researchers] found that these dual-potential stem cells can be identified and potentially isolated from other liver cells." |
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| You might recall that age-related thinning of the myelin that insulates nerves strongly correlates with declining brain function. Researchers investigating MS are making progress into the mechanisms by which this happens: the protein netrin-1 "is known to guide and direct nerve cell axons to their targets. ... blocking the function of netrin-1 and one of its receptors in adult neural tissue causes the disruption of myelin. ... We've known for just over 10 years that netrin is essential for normal development of the nervous system, and we also knew that netrin was present in the adult brain, but we didn't know why. ... the new findings show that netrin-1 and its receptor are needed to hold paranodal junctions in place, and thereby maintain the structure of myelin. The paranodal junction is a highly specialized region of contact where an oligodendrocyte cell attaches itself to the nerve cell's axon. This juncture acts as a molecular fence, which organizes and segregates the distribution of key proteins along the nerve cells axon and plays an imperative role in the proper conduction of electrical signals along the length of the nerve cell. When the function of netrin-1 and its receptor is disrupted, the organization of this adhesive junction comes apart, disrupting the function of nerve cells in the brain and spinal cord." |
| From the Economist: "a second generation of nanoparticles has entered clinical trials. Some are so good at hiding their contents away until they are needed that the treatments do not merely reduce side-effects; they actually allow what would otherwise be lethal poisons to be supplied to the tumour and the tumour only. Others do not depend on drugs at all. Instead, they act as beacons for the delivery of doses of energy that destroy cancer cells physically, rather than chemically. ... To get them to the cancer, you whip up a batch of, say, 80 trillion of them and inject it into the patient's bloodstream. The particles end up in the tumour, rather than in healthy tissue, because tumours have abnormal blood capillaries. The pores in these vessels are larger than those in healthy tissues. Make your nanoshells the right size, then, and they can pass through the capillary pores and lodge in a tumour, but not in a normal organ. Twelve to 36 hours later, when enough shells have accumulated, you insert an optical fibre into the tumour, and deliver an appropriate blast of infra-red. That heats the particles up and cooks the tumour." |
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| The fifth Hourglass blog carnival on the science of aging and longevity is hosted at psique: "It seems that prohibiting olfaction pharmacologically, by ablation of olfactory regions or genetic manipulation can result in an extension of life span, at least in C. elegans and Drosophila. Interestingly, [calorie restriction (CR)] and blocking olfaction appear to act in synergy, increasing life span most effectively when applied together, while exposure to food odours is capable of reducing the positive effects of CR to some extent. The obvious question is whether losing the sense of smell could also extend life span in humans. Failing the possibility of clogging up people's noses, Plunet proposes a straightforward test - one could compare the life span of anosmics, who are people that have chronically lost their ability to smell for a variety of reasons, to carefully matched controls." |
| Via the Daily Galaxy: biomedical gerontologist "Aubrey de Grey has famously stated, 'The first person to live to be 1,000 years old is certainly alive today ... whether they realize it or not, barring accidents and suicide, most people now 40 years or younger can expect to live for centuries.' Perhaps de Gray is way too optimistic, but plenty of others have joined the search for a virtual fountain of youth. In fact, a growing number of scientists, doctors, geneticists and nanotech experts - many with impeccable academic credentials - are insisting that there is no hard reason why ageing can't be dramatically slowed or prevented altogether. Not only is it theoretically possible, they argue, but a scientifically achievable goal that can and should be reached in time to benefit those alive today. ... But not everyone thinks ageing can or should be cured. Some say that humans weren't meant to live forever, regardless of whether or not we actually can." From there the piece leads into a rogue's gallery of quotes from pro-death advocates who want to see us all age, decay, and slowly, painfully die. |
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| A very readable overview of recent research from PLoS Biology: "When resources are short, growing organisms face an existential choice: should you ignore the shortage and hope for better times soon, or scale back and live within your limited means? And if you do scale back, will there be any payoff later in life? For animals, these choices are played out hormonally, with environmental fluctuations leading to internal rearrangements in endocrine signal and response throughout the growing body. In mammals, two principal hormones - growth hormone (GH) and insulin-like growth factor 1 (IGF-1) - promote growth. Remarkably, inhibiting one or both of these two not only retards growth, but also extends lifespan, not just in lab animals, but possibly also in people: mutations that reduce the function of the IGF-1 receptor have recently been discovered in centenarians (who are also short). Growth occurs throughout the body, and receptors for IGF-1 are found in every organ on virtually every cell. But [researchers have now shown] that it is the IGF-1 receptors in the brain that set the pattern for growth and lifespan." |
| An interesting, if flawed, article on the singularity and engineered longevity via the Korean OhmyNews: "Amidst the rapid changes of society ranging from general advances in science and technology to politics and social policy, with respect to knowledge, there is an emergent issue that promises to radically change our lives and our reality. It is predicted that within less than 20 years, the human lifespan will be extended to perhaps 150 or more years. Scientists and futurists on the cutting edge of thought about science and society believe that the increase in lifespan is one step towards what will be known as the Singularity, at which time, life might be extended indefinitely depending upon environmental conditions. The Singularity is the term used for a technological integration unheard of; it is a theoretical future point of unprecedented technological progress, caused in part by the ability of machines to improve themselves using artificial intelligence. ... it was just over a hundred years ago, when the human lifespan began to double to what it is today. It is possible that most people who lived only to 35 years of age thought that to live to 72 years would be too long and that they would be too tired. Nevertheless, we have adjusted and found life to be meaningful, even in our current 'long' life of 72 years." |
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| From the Exchange Morning Post, a statist, public funding viewpoint on longevity science: "Learning how to turn back time - or at least how to slow the aging process - may be more important for improving our overall health than the discovery of a cure for cancer ... there are real, tangible benefits, for society as well as individuals, to slowing down the aging process. 'By extending the life span, people would remain in the workforce longer, personal income and savings would increase, age entitlement programs would face less pressure from shifting demographics, and national economies would flourish' ... almost half of the current population over 75 years old is limited in their activity by chronic conditions, with costs to society set to rise dramatically ... Given the current predicament we face, we can't ignore the call to tackle aging more aggressively. To those who ask: 'Can we really afford to invest more in such research?' we can reply: 'Can we really afford not to tackle aging?' ... the greatest obstacle will be convincing the general public that slowing the aging process is both feasible and deserving of a larger share of the funds available for scientific research." |
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