They headed off heart disease not by preventing the gene mutation, but by correcting its consequence, sparking hope that drugs can be developed to do that, too, by going after the genetic pathway, Benjamin said.

Cells normally consume about 95-98 percent of oxygen through biochemical pathways that typically don't harm the cells. The small percent of oxygen they can't handle generates a reactive oxygen species, or free radicals, that do oxidative harm. That's why antioxidants are believed to prevent heart and other protein-aggregate diseases, although there's not much evidence to prove they work, Benjamin said.

Treatments could be a decade away, he said, but he's optimistic. "I think if we're able to find new compounds that can inhibit this pathway and we are able to find other human conditions where this type of strategy might work, we may well be onto breakthroughs for intractable conditions."

Study co-authors include Namakkal S. Rajasekaran, Ph.D, Andras Orosz, Ph.D., Ryan P. Taylor, Ph.D., Xia Q. Zhang, Ph.D., Tamara J. Stevenson, Dr. William H. Barry and Shannon J. Oldelberg, Ph.D, all from the U. School of Medicine; Patrice Connell, Ph.D., Liang-Jun Yan, Ph.D., Elisabeth S. Christians, D.V.M., Ph.D., and Dr. Ronald M. Peshock, M.D., the University of Texas Southwestern Medical Center, Dallas; and Dr. Jane A. Leopold and Dr. Joseph Loscalzo, Harvard Medical School. Christians also is associated with the Centre for Developmental Biology, Toulouse, France.

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