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A team of University of Michigan scientists has found that suppressing a newly discovered gene lengthens the lifespan of roundworms. Scientists who study aging have long known that significantly restricting food intake makes animals live longer. But the goal is to find less drastic ways to achieve the same effect in humans someday. The U-M results offer promising early evidence that scientists may succeed at finding targets for drugs that someday could allow people to live longer, healthier lives.
In a study in the August issue of Aging Cell, U-M scientists found that a gene, drr-2, is an important component in a key cellular pathway, the TOR nutrient-sensing pathway, where many scientists are looking for potential drug targets. The U-M scientists then found that when they caused the drr-2 gene to be under- or over-expressed, they could lengthen or shorten lifespan in C. elegans, a worm widely used in research. Manipulating the drr-2 gene’s action produced the same effects as reducing or increasing caloric intake.
By analyzing just 150 spots on the genome, researchers can predict who will live to extreme old age with almost 80 percent accuracy, according to a study published online today in the journal Science. Researchers from Boston University employed a widely used genetic-screening technology to find genetic variations that occur more frequently in centenarians–people age 100 and older. In addition to providing a potential way to predict who might live into their 100s, the findings suggest that genetics play a major role in surviving to extreme old age. And the team hopes that identifying the genes and corresponding molecular mechanisms that promote longevity will give new insight into how to prevent or delay age-related diseases, such as heart disease, Alzheimer’s, and cancer. “Centenarians are a model of aging well,” says Thomas Perls, director of the New England Centenarian Study at Boston Medical Center and an author of the study. Previous findings from the project, the largest study of centenarians in the world, show that 90 percent of them are free of disability to an average age of 93. “They seem to compress disability to the end of their lives,” says Perls. “I am very hopeful that understanding how centenarians do that will lead to new strategies for therapies.” Perhaps most surprisingly, preliminary analysis showed that centenarians had just as many genetic variants linked to diseases as did people in the control group. “That suggests that what makes people live long lives is not lack of genetic disposition to disease but longevity-promoting genes,” says Paola Sebastiani, a biostatistician at Boston University and coauthor of the study. “If longevity variants cancel out disease-associated variants, it could open new ways of treating age-related diseases.”
“Centenarians are a model of aging well,” says Thomas Perls, director of the New England Centenarian Study at Boston Medical Center and an author of the study. Previous findings from the project, the largest study of centenarians in the world, show that 90 percent of them are free of disability to an average age of 93. “They seem to compress disability to the end of their lives,” says Perls. “I am very hopeful that understanding how centenarians do that will lead to new strategies for therapies.”
Perhaps most surprisingly, preliminary analysis showed that centenarians had just as many genetic variants linked to diseases as did people in the control group. “That suggests that what makes people live long lives is not lack of genetic disposition to disease but longevity-promoting genes,” says Paola Sebastiani, a biostatistician at Boston University and coauthor of the study. “If longevity variants cancel out disease-associated variants, it could open new ways of treating age-related diseases.”
