The Nobel Prize for medicine has been awarded to three U.S. researchers who probed the mechanism of cellular division, and whose work opened new avenues both in the fight against cancer and attempts to slow aging. The prize will be shared by Australia-born Elizabeth Blackburn, Carol Greider, and London-born Jack Szostak.
The three researchers solved the mystery of how chromosomes, the rod-like structures that carry DNA, protect themselves from degrading when cells divide. The Nobel citation said the laureates found the solution in the ends of the chromosomes — features called telomeres that are often compared to the plastic tips at the end of shoe laces that keep those laces from unraveling [AP].
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Babies born in rich nations today have the best shot at becoming centenarians. That’s if current life expectancy trends continue, according to the study published in The Lancet.
Not only will these babies live longer, but they’ll be healthier well into old age. The researchers based their projections on a case study of Germany that showed that by 2050, its population will be substantially older and smaller than now — a situation it said was now typical of rich nations [Reuters]. In the United States, half of the babies born in 2007 are expected to live to a ripe 104 years old. The authors credited improvements in health care, medicine, and lifestyle, as well as a drop in infant mortality rates, for increased life spans.
Data from more than 30 developed countries shows that since 1950 the probability of surviving past 80 years of age has doubled for both sexes [BBC News]. However, the study cautions that despite improved life expectancies, an increase in cancer, cardiovascular disease and other chronic illnesses has risen with aging populations [ABC News]. As citizens get older and require more medical care, the increased life expectancies may place a burden on society. Already, many countries are pushing to extent the retirement age to grapple with the costs.
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80beats: A Single Genetic Tweak Gives Mice Longer, Healthier Lives
80beats: Low-Calorie Diet Staves off Aging & Death in Monkeys
Image: flickr / Will Foster
By deleting a single gene from a mouse’s genetic makeup, researchers have created a mighty mouse with a longer, healthier life. The change mimicked the effect of keeping the mice on a calorie-restricted diet. Severely restricting the diets of yeast, bacteria, mice and primates have granted these animals unnaturally long lives. For humans, however, maintaining a diet of near starvation would be difficult at best [Discovery News]. That’s why researchers are actively pursuing drugs that could produce the same anti-aging effect.
Study coauthor Dominic Withers says the effect was striking–but for reasons not yet understood, only the female mice benefited. The mice didn’t just live longer, they also had fewer age-related ailments. “These mice were resistant to type 2 diabetes … and they also appeared to have reduced incidence of the mouse-equivalent of osteoporosis — so they had stronger bones,” Withers said. Balance, strength and coordination all improved in the [female] mice, and they were more inquisitive, suggesting their brains were healthier [Reuters].
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One of Britain’s best-known orchestra conductors and his wife have ended their lives at an assisted suicide facility, reigniting the debate over assisted suicide. Helping someone die is a criminal offense in Britain, so Sir Edward Downes, 85, traveled to a “right-to-die” facility near Zurich with his 74-year-old wife, Joan, who had terminal cancer.
Under Britain’s Assisted Suicide Act, helping someone kill him- or herself can bring a penalty of up to 14 years in prison. In Switzerland, however, assisted suicide is legal; the Downeses were not the first Britons who traveled there to legally commit assisted suicide. Since the Zurich clinic run by [the non-profit group] Dignitas was established in 1998 under Swiss laws that allow clinics to provide lethal drugs, British authorities have effectively turned a blind eye to Britons who go there to die…. None of the family members and friends who have accompanied the 117 people living in Britain who have traveled to the Zurich clinic for help in ending their lives have been charged with an offense [The New York Times]. Experts say it’s unlikely that this will change in the case of the Downses’ children, who potentially assisted in their parents’ suicide by traveling with them to the Zurich facility. Still, the fact remains that the couple’s children could potentially be charged with a crime for their involvement in the suicide.
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A new study based on neurological data and brain specimens from a group of nuns, known as the Nun Study, confirms that language skills earlier in life are linked to Alzheimer’s disease risk in older age. But it also adds new, puzzling information to our knowledge about the disease: The brains of the women who did not have Alzheimer’s symptoms had larger brain cells, or neurons, but not necessarily fewer of the plaques and tangles characteristic of the disease.
To assess language skills early in life, researchers examined essays written by 14 women when they entered the convent, looking for the number of ideas expressed in every group of 10 words. A previous study linked grammatically complex writing skills to a decreased risk of dementia, and this study confirmed it: The essays written by women who maintained their memory scored 20 percent higher on language tests. “This is the second independent sample with the same result. We’re back to the metaphor of the brain as a computer and a muscle,” said [geriatric psychiatrist] Dr. Gary J. Kennedy…. “In volunteers who had no signs of Alzheimer’s but did have the plaques and tangles, the neurons were actually larger and more functional with more connections” [U.S. News and World Report].
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It’s been a big week on the longevity front: First, scientists found that an immunosuppresant drug called rapamycin extended the lifespan of mice. Now, a 20-year-long study reported in the journal Science shows that a diet 30 percent lower in calories than normal decreased the incidence of age-related diseases in macaque monkeys as the animals got older.
Half the monkeys were fed a low-calorie diet, and the other half a standard diet. All were closely monitored, with researchers regularly measuring their body composition, blood chemistry, endocrine function, and heart and brain function. When monkeys died, they were necropsied and the causes of death established [Wired.com]. Researchers found that monkeys on a calorie-restricted, nutrient-rich diet (on the left in photo) were three times less likely than monkeys on a full-calorie diet (on the right) to die from age-related diseases like cancer, diabetes, and heart disease. Scientists have hypothesized that calorie restriction triggers mechanisms that evolved to help organisms survive in times when food was scarce, but the exact process is still mysterious.
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Laboratory mice who were given an immunosuppresant drug called rapamycin lived between 9 and 14 percent longer than mice who didn’t take the drug, according to a study in Nature. The drug, which was developed from bacteria found in Easter Island’s dirt, is the first pharmacological agent shown to enhance longevity in a mammal [Technology Review]. Even more remarkable, the mice weren’t given the drug until late middle age, showing rapamycin had effects even when taken later in life.
The drug is already used to suppress the immune systems of organ transplant patients, and it’s undergoing clinical testing as a possible cancer treatment. Rapamycin works by inhibiting the target of rapamycin (TOR) signaling pathway, which plays a role in the translating mRNA into proteins and inhibits processes that degrade cellular waste. The drug has been found to extend the life spans of yeast, fruit flies, and nematodes [The Scientist], but this is the first time it’s been shown to help mammals live longer. The drug boosted the lifespans of mice that were 600 days old at the time of treatment, the equivalent in age to a 60-year-old human. “That is very surprising to myself and to a lot of people,” [said pathologist Matt] Kaeberlein. “And it’s a very important result” [The Scientist]. However, it still isn’t clear exactly how the TOR signaling pathway is involved in the aging process.
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The notion that stress can cause hair to turn gray isn’t entirely a myth: at least when it comes to genetic stress applied to laboratory mice. That’s what researchers found when they damaged mice’s DNA with ionizing radiation, according to a study published in the journal Cell.
Scientists already knew that cells known as melanocyte stem cells were responsible for youthful hair color. Each of these cells divides into two cells: One that replaces itself and another that differentiates into a pigment-producing daughter cell called a melanocyte, which imbues hair with its browns, reds and blacks. Earlier research has suggested that the depletion of these stem cells was to blame for grayness. But how exactly these stem cells disappeared was mysterious. With no more stem cells around to produce melanocytes, hair turns gray [Science News].
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The Greek poet Homer was first to make written reference to a “sardonic smile,” and in the millennia since the phrase has been used to denote a bitter or cynical grin. Now, researchers in Italy say they’ve discovered a poisonous herb that gave rise to Homer’s coinage: a plant called hemlock water-dropwort that grows wild across the island of Sardinia and was used in the ancient Sardinians’ death rituals. The plant was used in pre-Roman times for the ritual killing of old people who had become a burden to society. “According to ancient historians, elderly people unable to support themselves were intoxicated with the herb and then killed by being dropped from a high rock or by being beaten to death,” the research team wrote [Telegraph]. The plant’s toxins can cause facial muscles to contract, researchers note, leaving an eerie smile frozen on the face of the corpse.
The poet Homer first used the word ‘sardonic’ as an adverb when describing Odysseus’ smile. The Greek hero “smiled sardonically” as he dodged an ox jaw thrown by one of his wife’s former suitors. According to some scholars, Homer coined the word after learning that the Punic people who settled Sardinia gave condemned people the smile-inducing potion [Discovery News].
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Spikes in blood sugar levels seem to be linked to memory problems, and may be a major factor in the normal memory and cognitive problems that crop up as people age, according to a new study. People’s ability to regulate blood sugar begins to deteriorate by their third or fourth decade and continues to decline, so older people are more prone to these sugar spikes. “This would suggest that anything to improve regulation of blood glucose would potentially be a way to ameliorate age-related memory decline,” said senior study author Dr. Scott Small…. The findings may also help explain why people who exercise don’t have as many cognitive problems as they age: Exercise helps stabilize blood glucose levels [HealthDay News].
The findings have important implications for the increasing number of overweight children who are at risk of diabetes, commented neuroscientist Bruce McEwen. “When we think about diabetes, we think about heart disease and all the consequences for the rest of the body, but we usually don’t think about the brain,” he said. “This is something we’ve got to be really worried about. We need to think about their ultimate risks not only for cardiovascular disease and metabolic disorders, but also about their cognitive skills, and whether they will be able to keep up with the demands of education and a fast-paced complex society. That’s the part that scares the heck out of me” [The New York Times].
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Researchers may have uncovered one of the universal causes of aging: A crucial type of protein that serves a double duty in organisms ranging from yeast to mice, and that becomes overwhelmed as the organism ages. The protein is charged both with repairing DNA damage and with regulating gene expression (so that, for example, a gene necessary for liver function doesn’t suddenly get turned on in the brain), and a new study has shown that when the protein is busy repairing DNA, it can’t perform its other task. Says lead author David Sinclair: “One idea of why we age is that DNA becomes damaged or mutated…. But perhaps the main culprit is the effect of genes switching on and off, and that should be reversible” [Wired News].
About a decade ago, researchers identified a protein called Sir2 that zooms to the spot of broken DNA in yeast cells and repairs the breaks. But to do that, Sir2 has to abandon its job of inactivating a sterility gene elsewhere in the yeast genome. The result is yeast cells that have intact DNA but are sterile, a symptom of aging in the fungi…. “This may be a very fundamental Achilles’ heel of life,” says Sinclair [ScienceNOW Daily News]. Now, Sinclair’s team has identified the mammalian equivalent of that protein, called SIRT1, and have determined that it plays a similar role in aging mice: When it focuses on repairing DNA damage, it neglects its gene regulation duties.
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A hormone produced in the gut appears to limit bone formation, scientists report in Cell [subscription required]. The hormone, serotonin, is the same one produced by the brain to regulate mood, learning, and sleep, but the new study finds that serotonin produced by the gut has an entirely separate function. Mice engineered to produce extra serotonin formed weak bones, while mice engineered to produce less serotonin developed extra-strong bones. The research, though still basic, suggests new avenues of osteoporosis research in humans. “It’s what you’d call a landmark study,” Bjorn Olsen [a Harvard cell biologist who was not involved with the study] says. “It opens new doors” [Science News].
Although serotonin produced by the gut makes up 95 percent of the body’s serotonin, its function had not been well understood. The connection between serotonin and bone formation revealed itself through two types of rare human diseases, both involving the gene Lrp5. People with one mutation produced less Lrp5 protein, developing fragile bones and blindness, while people with another mutation produced extra Lrp5 protein, developing unusually dense bones and resistance to osteoporosis. However, when the authors of the new study looked into the gene further, they were surprised to find that it acted not in bone cells but in cells of the gut. “We, as bone [researchers], thought of the skeleton as functioning independent of everything else,” said [Cliff Rosen, a bone biologist]. This group “asked the question, ‘could there be other regulators outside the skeleton that are regulating bone?’ and found the answer to be ‘yes.’” [The Scientist].
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Contrary to conventional wisdom, marijuana may actually fight memory loss, scientists report—but only if taken in small doses amounting to just one puff a day. Researchers tested a compound similar to THC, the main psychoactive substance in marijuana, on rats and found that the chemical reduces inflammation in the brain and promotes the growth of new brain cells. Elderly rats given the compound performed better on learning and memory tasks. “Could people smoke marijuana to prevent Alzheimer’s disease if the disease is in their family? said [researcher Gary Wenk]. “We’re not saying that, but it might actually work” [Telegraph].
In one part of the study, researchers injected the THC-mimicking drug, called WIN-55212-2, into young rats with inflammation in their brains. The drug reduced inflammation. In a second part, the researchers injected WIN into older rats that were then put into a swimming tank with hidden resting spots. The medicated rats were better able to find and remember the resting spots. Dissection of the rat brains revealed not only reduced inflammation but the growth of new neurons. The results were presented at last week’s Society of Neuroscience meeting.
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In yet another warning signal of the toll that childhood obesity will take on health and health care budgets, a small study has shown that overweight kids as young as 10 years old have the thickened arteries of 45-year-olds. Researchers say the findings raise the possibility that these kids could develop serious heart disease in their 20s or 30s. “There’s a saying that ‘you’re as old as your arteries,’ meaning that the state of your arteries is more important than your actual age in the evolution of heart disease and stroke,” said [lead researcher] Dr Geetha Raghuveer [Telegraph].
The findings, while preliminary, should serve as a serious alarm bell in the United States, where about one-third of children are overweight and almost one-fifth are obese. Many parents think that “baby fat” will melt away as kids get older. But research increasingly shows that fat kids become fat adults, with higher risks for many health problems. “Obesity is not benign in children and adolescents,” said Dr. Robert Eckel, a former heart association president [AP].
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Honda’s robotics division has unveiled the prototype of a strange new helper: a “walking assistant.” Honda says the robotic legs could restore mobility to the elderly or infirm, and could help prevent factory workers from straining their muscles–if they don’t mind being joined to the strange looking device. The user would employ the device by stepping into a pair of shoes attached to jointed legs. The legs support a mildly-scary looking U-shaped saddle, which cups the wearer’s groin and buttocks firmly to deliver solid uplift…. Honda say that the machine reduces load on the hip joints, and helps not just with walking but also standing – and especially with maintaining a crouched position [The Register].
The device, which weighs about 14 pounds and is powered by a motor and Lithium ion battery, is the result of Honda’s nine-year-old initiative to develop mobility-assisting technologies. The creation of the device borrowed heavily from the walking research that went into Honda’s advanced humanoid robot, ASIMO [Daily Tech]. Honda hasn’t yet announced plans to begin selling the walking assistants, but tests of the prototype will begin this month.
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