| Exercise mimetics? The benefits of working out, in pill form.As a biologist of aging, one question I get asked frequently is: “What pills should I be popping?” My answer: Supplements are of questionable value, but the old advice is still good advice: Avoid tobacco, eat a reasonable diet, and get plenty of exercise. After all, I usually jest, they’re never going to turn exercise into a pill. Until, you know, they do. |
| Hourglass II: A blog carnival devoted to the biology of agingThe second issue of Hourglass, a carnival of biogerontology, includes posts about endocrine control of aging, the retasking of anticancer therapies as anti-aging therapies, and meditations on the role of environment in determining optimal lifespan. |
| How degrading: The role of protein turnover and autophagy in agingAs cells age, detritus inevitably accumulates; one theory of aging holds that rising levels of unwanted molecules will eventually become cytotoxic; this, in turn, could cause age-related decline in tissue function. Cells have a variety of means to eliminate misfolded, damaged and covalently altered proteins; here is a review of some recent articles on the role of these mechanisms in aging -- including one idea about how this knowledge might be incorporated into life extension technology. |
| No end to telomeres: a glancing review of recent literatureTelomeres shorten with every cell division, essentially providing a “clock” that ticks down until reaching some critical length, at which point the cell will undergo the permanent growth arrest known as senescence; senescent cells themselves contribute both directly and indirectly to aging. Telomere length is also a useful biomarker: it is positively correlated with life expectancy, and appears to respond to environmental influences including chronic infection and psychological stress. |
| Keeping up with IGF-I and FOXOThe insulin-like growth factor-I (IGF-I) pathway is involved in regulating healthspan and lifespan; the FOXO transcription factors are essential for the relevant effects. Here is a quick review of a half-dozen recent articles on the roles of this pathway in cancer, stem cell biology, and other aspects of aging and disease. |
| How a single-celled organism is unlocking the secrets of mammalian agingOur understanding of aging in animals owes a great debt to a large body of careful work in a single-celled organism, the brewer’s yeast Saccharomyces cerevisiae. Indeed, as I’ve argued before, yeast is one of the two organisms with the strongest credible claim to have started modern biogerontology. An unusually large crop of yeast aging papers have appeared over the last few months, and I thought it would be appropriate to spend a few paragraphs describing them... |
| Calcium and Alzheimer's diseaseTwo related findings that surely signal a major new direction in the study of Alzheimer’s disease (AD): Two means of controlling intracellular calcium homeostasis appears to play a major role in controlling levels of the Aß protein, a major component of the senile plaques that characterize AD and (thusly) a likely source of AD-associated cell death. Specifically, deficiencies in two distinct calcium pumps appear to promote molecular events associated with AD pathology. |
| Sugar-modified proteins associated with aging may cause DNA damageOver the lifespan, many proteins are modified by carbohydrates to form so-called AGEs (advanced glycation endproducts). These compounds have long been associated with aging. New data suggests that AGEs may cause damage to DNA, suggesting a molecular mechanism for the role of AGEs in age-related cellular decline. |
| In the naked mole rat, stress responses help test models of agingIn most organisms studied, response to cellular stress predicts longevity: greater stress resistance correlates with greater longevity. In the naked mole rat, however, stress resistance follows an unusual pattern: Even though these odd animals live ten times longer than similarly sized rodents, they are hypersensitive to certain stressors. These observations have significant ramifications about models of how aging works in mammals. |
| Evolutionary theories of aging, as applied to lifespan extensionMultiple factors contribute to aging, including the accumulation of molecular damage, but also the failure of organisms to adapt to their age-specific "fitness landscape". A prominent evolutionary biologist and theorist of aging argues that successful lifespan extension will require attention to the factors that determine these age-specific losses in fitness. |
| Aging and disease as modifiers of stem cell therapyStem cells hold great promise as therapeutics, but unfortunately aged tissues are often hostile environments for stem cell growth. We're beginning to understand, in molecular detail, the reasons why stem cells struggled in aged tissues, and what we might do to correct the problem. |
| DNA damage as a cause of agingDoes DNA damage cause aging, and if so, how? Two recent articles by a prominent scholar in the field conclude that a dangerous sort of DNA damage known as double-strand breaks (DSBs) are causative forces in aging -- and that the body's defenses against DSBs evolved primarily as a defense against aging, not cancer. |
| Low doses of resveratrol still have anti-aging and health benefitsThe natural product resveratrol, derived from wine grapes, has been touted as a possible life-extension drug. Previous studies in mice, however, have used such high doses of the compound in highly unnatural dietary backgrounds, raising questions about the applicability of their results to human health. A new study, however, has used a more natural diet and more realistic doses of resveratrol, and the results are still promising. Specifically, resveratrol appears to delay aging in much the same way as calorie restriction, a documented means of extending lifespan in multiple species. |
| Sirtuins and resveratrol come under fireA widely held theory of aging holds that enzymes called "sirtuins" regulate lifespan, and that these proteins can be activated by small molecules such as resveratrol. As the theory approaches maturity, challenges are emerging, some of which question the entire basis of the idea. |
| Personalized aging prevention?We're coming to realize the importance of personalized programs for prevention and treatment of cancer. The authors extrapolates from oncology to biogerontology, and argues that an analogous personalization (i.e.,taking into account the idiosyncrasies of aging in specific individuals) will have to occur in order for future anti-aging technologies to be effective. |
| "The Stupidity of Dignity""Human dignity" is sometimes deployed as a justification against pursuing research that would improve prospects for health and longevity. Linguist Steven Pinker has recently challenged this idea. In this post, a blogger discusses Pinker's article from the perspective of biogerontology and life extension technologies. |
| Calorie restriction may be psychologically beneficial to humansEarly results showed that calorie restriction, which delays aging, caused anxiety and depression in mice and rats. New data suggest that this phenomenon may be limited to rodents, and that CR has neutral or beneficial psychological effects in human beings. |
| Chronic infection shortens telomeresThe lengths of telomeres, stretches of DNA at the ends of chromosomes, have been used as a biomarker for aging: increased age is associated with shortened telomeric DNA. Shortened telomeres have also been suggested to have a causative role in the aging process.
New data obtained in mice reveals that chronic infection can shorten telomeres, suggesting a mechanism by which stress could affect telomere length and also implying that disease over the lifespan could contribute to immunological aging. |
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