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Archive - Feb 7, 2010


First Genetic Variants Associated with Biological Aging in Humans

Scientists announced that they have identified, for the first time, definitive genetic variants associated with biological aging, as indicated by mean telomere length, in humans. An international team, led by researchers at the University of Leicester and King’s College London, analyzed more than 500,000 genetic variations across the entire human genome to identify the aging-related variants which are located near a gene called TERC, a gene that is known to play a role in telomere length. Telomeres are capping-like structures located at the tips of chromosomes. “Individuals are born with telomeres of certain length and in many cells telomeres shorten as the cells divide and age,” said Dr. Nilesh Samani, a co-leader of the project. “Telomere length is therefore considered a marker of biological aging." Dr. Samani explained that there are two forms of aging--chronological aging, i.e., how old you are in years, and biological aging whereby the cells of some individuals are older (or younger) than suggested by their chronological age. “In this study,” Dr. Samani said, “what we found was that those individuals carrying a particular genetic variant had shorter telomeres, i.e., looked biologically older. Given the association of shorter telomeres with age-associated diseases, the finding raises the question whether individuals carrying the variant are at greater risk of developing such diseases." Dr. Tim Spector, also a co-leader of the project, noted, “What our study suggests is that some people are genetically programmed to age at a faster rate. The effect was quite considerable in those with the variant, equivalent to between 3-4 years of 'biological aging’ as measured by telomere length loss.

Serotonin Inhibitor Appears to Cure Osteoporosis in Rodents

An investigational drug that inhibits serotonin synthesis in the gut effectively cured osteoporosis in mice and rats when administered orally once a day, according to a report by an international team led by researchers from the Columbia University Medical Center. "New therapies that inhibit the production of serotonin in the gut have the potential to become a novel class of drugs to be added to the therapeutic arsenal against osteoporosis," said Dr. Gerard Karsenty, Chair of the Department of Genetics and Development at the Columbia University College of Physicians and Surgeons, and a senior author of the report. "With tens of millions of people worldwide affected by this devastating and debilitating bone loss, there is an urgent need for new treatments that not only stop bone loss, but also build new bone. Using these findings, we are working hard to develop this type of treatment for human patients." The current study followed up on an earlier report, in Cell (November 28, 2008), by Dr Karsenty’s group and colleagues, showing that serotonin released by the gut inhibits bone formation, and that regulating the production of serotonin within the gut affects the formation of bone. Prior to that discovery, serotonin was primarily known as a neurotransmitter acting in the brain. Yet, 95 percent of the body's serotonin is found in the gut, where its major function is to inhibit bone formation (the remaining 5 percent is in the brain, where it regulates mood, among other critical functions). By turning off the intestine's release of serotonin, the team was able, in the new study, to cure osteoporosis in rodents that had undergone menopause. The results demonstrated that osteoporosis was prevented from developing, or when already present, could be fully cured.