Suppressing a newly discovered gene, drr-2, lengthens the lifespan of roundworms without reducing caloric intake, University of Michigan scientists have found.

Scientists who study aging have long known that significantly restricting food intake makes animals live longer, due to less oxidative damage in animal cells and a slower decline in DNA repair, a decline that normally occurs with age. It’s thought that limiting oxidative damage and slowing the decline in DNA repair could help postpone or avoid many age-related diseases.

But to achieve anti-aging benefits, it’s thought that people would have to restrict food intake by 30 to 40 percent, a grim prospect. In addition, drugs might be designed to avoid other disadvantages of this level of dietary restriction, which include reduced fertility.

So 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 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.

The study also found that drr-2 appears analogous to a human gene, eIF4H, that controls similar cell functions.

Funding: Ellison Medical Foundation and the National Institutes of Health Citation: DOI: 10.1111/j.1474-9726.2010.00.

More info: University of Michigan news