Reducing single gene activity boosts healthy longevity in mice: study

A reduction in the function of a fundamentally important gene called Myc may significantly increase the healthy lifespan of laboratory mice, a U.S. study said Thursday.

Myc, found in the genomes of all animals, has been shown to be a central regulator of cell proliferation, growth and death. It is of such widespread and fundamental importance that animals cannot live without it, said the study in the U.S. journal Cell.

But in humans and mice, too much expression of the protein that Myc encodes has been closely linked to cancer, making it a well- known but elusive target of drug developers, according to the study led by researchers at the Brown University.

In the study, researchers bred laboratory mice to have only one copy of the gene, instead of the normal two, thus reducing the expression of the encoded protein.

They found those mice lived 15 percent longer on average -- 20 percent longer for females and 10 percent longer among males -- than normal mice. It's the first time the gene has been shown to boost lifespan in a mammalian species.

More importantly, the experimental mice showed many signs of better health into old age.

"These mice are incredibly normal, yet they are really long- lived," said senior author John Sedivy, professor of medical science at Brown University.

"The reason why we were struck by that is because in many other longevity models like caloric restriction or treatment with rapamycin, the animals live longer but they also have some health issues."

The experimental mice did not develop osteoporosis, they maintained a healthier balance of immune system T cells, had less cardiac fibrosis, were more active, experienced less age-related slowing of their metabolic rate, produced less cholesterol, and exhibited better coordination, the study said.

The only problem was mice grew to be about 15 percent smaller than the normal mice,a probable disadvantage in the wild,Sedivy said.

The study found those mice exhibited changes in several pathways known to be involved in regulating longevity but how Myc engages those mechanisms is still not clear.

In the long term, Sedivy said he is optimistic that the findings might help people stay healthier as they age, such as reducing osteoporosis in people.

The study also offered encouragement to companies seeking to develop cancer drugs that block Myc overexpression as drugs that target Myc directly are likely to find many applications beyond cancer, he added. Endite