London — Researchers here say they have found a way to extend the lifespan of mice and, possibly, humans, reports news source AFP.com.
In a recently released study, scientists from the Institute of Healthy Aging at University College London (UCL) say the key to prolonged youth lies in genetic manipulation that mimics the health benefits of reduced calorie intake. The study was published in a recent issue of the journal Science.
The authors write that decades ago scientists first showed that reducing calorie intake by 30 percent can be beneficial for rats and mice. A more recent finding suggests that similar calorie-intake reductions can extend primates’ lifespan by 40 percent and have significant health benefits.
In their study, the researchers were able to extend the lifespan of mice by as much as 20 percent—while at the same time reducing incidence of age-related diseases in the rodents—by genetic manipulation that blocks production of the S6 Kinase 1 (S6K1) protein. By blocking S6K1, which is involved in the body's response to changes in food intake, similar benefits were obtained without reducing food intake, according to the study.
AFP.com quotes UCL professor Dominic Withers, the study’s lead author, as saying, "The results corroborated those of other recent studies. Blocking the action of the S6K1 protein helps prevent a number of age-related conditions in female mice. The mice lived longer and were leaner, more active and generally healthier than the control group."
The study’s genetically altered female mice lived 20 percent longer than mice in the control group. At age 600 days — the equivalent of middle age in humans — the altered mice were leaner, had stronger bones, were protected from type-2 diabetes, performed better at motor tasks, and displayed higher levels of sensory and cognitive ability.
In addition, the altered rodents’ T-cells—key components of the immune system—appeared more "youthful," which according to the study indicates that the rate of decline in immunity that usually accompanies aging was slowed.
AFP.com quotes co-author David Gems, of UCL’s Institute of Healthy Aging, as saying, "We are suddenly much closer to treatments for aging than we thought. We have moved from initial findings in worm models to having ‘druggable’ targets in mice. The next logical step is to see if drugs like metformin can slow the aging process in humans."
Metformin, already used in human patients to treat type 2 diabetes, also has been found to extend the lifespan of mice. The same is true for rapamycin, which is used in humans as an immunosuppresant to prevent rejection after organ transplants and could extend lifespan because it blocks S6K1 activity.
