Living to 150
Aubrey de Grey, British researcher on aging, believes that the person who will live to be 150 is alive today. He sees aging as a disease to be cured and presents the idea that maintenance can repair the prime causes of aging, extending life significantly.
While his ideas are considered controversial by some in the scientific community, new studies continue to reveal secrets that may one day prevent and reverse the diseases associated with aging. Science is telling us that many of the disorders that typically occur in old age are a result of disease processes, not normal aging.
Key Genetic Link in the Biology of Aging
Research at Oregon State University (OSU) suggests it may be possible to slow age-related disease with new types of treatments.
“Scientists have tracked the syndromes associated with aging to their biochemical roots, and identified a breakdown in genetic communication as part of the problem,” writes David Stauth of the Linus Pauling Institute at OSU. “The findings imply that aging happens for a reason, and that while aspects of it may be inevitable, there could be ways to slow down disease development.”
The study looks at a protein, Nrf2, that helps regulate the body’s reaction to various types of stressors. The research was published in Free Radical Biology and Medicine.
“We’re very excited about the potential of this area of research,” said Tory Hagen, the study’s author, and Professor for Health Aging Research in the Linus Pauling Institute.
“At least one important part of what we call aging appears to be a breakdown in genetic communication, in which a regulator of stress resistance declines with age,” Hagen said. “As people age and their metabolic problems increase, the levels of this regulator, Nrf2, should be increasing, but in fact they are declining.”
Nrf2 is constantly on the lookout for problems with cells that may be caused by the many metabolic insults of life – oxidative stress, toxins, pollutants and other metabolic dysfunction. It can “turn on” up to 200 genes that are responsible for cell repair, detoxification of carcinogens, protein and lipid metabolism, antioxidant protection and other actions. In their report, scientists called it a “longevity-assurance” factor.
Metabolic insults routinely increase with age, and if things were working properly, the amount of Nrf2 that goes back into the nucleus should also increase to help deal with those insults. Instead, the level of nuclear Nrf2 declines, and the OSU scientists say they have discovered why. The reason for this decline, the scientists said, is increasing levels of a micro-RNA called miRNA-146a.
Micro-RNAs have been one of the most profound scientific discoveries of the past 20 years. They were once thought to be “junk DNA” because researchers could see them but they had no apparent biological role. They are now understood to be anything but junk – they help play a major role in genetic signaling, controlling what genes are “expressed,” or turned on and off to perform their function.
The micro-RNA can turn on the inflammation processes that, in something like a wound, help prevent infection and begin the healing process. But with aging, this study now shows that it doesn’t shut down properly, causing part of the chronic, low-grade inflammation that is associated with the degenerative diseases that now kill most people in the developed world, including heart disease, cancer, diabetes and neurological disease.