Age-related hearing loss is known to be the most common sensory disorder among the elderly. However, researchers are still trying to discover what cellular processes seem to direct or contribute to the loss.
At present, researchers are believed to have recognized a protein that is essential to processes that cause oxidative damage to cells. In addition, they may lead to age-related hearing loss. The team of researchers was from University of Florida, University of Wisconsin and three other institutions.
One theory of aging holds that free radicals seem to damage components of mitochondria which are the energy center of cells. Such damage could perhaps collect over time thereby resulting in a destabilization of the mitochondria. Apparently, this destabilization of the mitochondria leads to release of certain proteins. Moreover, the cell death triggered by the escaped proteins appears to lead to physical effects which the researchers associate with aging, such as hearing loss.
“Within the mitochondria these proteins cause life, but when they’re out they’re deadly,†says Professor Christiaan Leeuwenburgh, chief of the biology of aging division at UF’s College of Medicine and a member of the Institute on Aging.
According to data from the National Health Survey, more than 40 percent of people in the United States older than 65 seem to suffer from age-related hearing loss. Furthermore, it is estimated that the condition will affect more than 28 million Americans by 2030.
“Because of the high prevalence of this disorder, AHL is a major social and health problem,†says Shinichi Someya, first researcher and a postdoctoral fellow in the group of Tomas Prolla of University of Wisconsin.
Age-related hearing loss supposedly, involves the death of certain sensory hair, nerve and membrane cells in the inner ear. Since the hair and nerve cells do not redevelop in humans, their death could perhaps lead to permanent hearing loss.
One protein called Bak is known to play a crucial role in the weakening of the mitochondrial membrane. If more protein is present, then the mitochondrial membrane tends to become leakier in turn allowing harmful proteins to travel out into the rest of the cell.
Bak seems to be typically induced by oxidative stress and its levels increase as people age. The researchers wanted to see whether its absence could prevent age-related hearing loss that is associated with the death of certain sensory hair, nerve and membrane cells in the inner ear.
Hearing tests showed that Bak-deficient middle-aged mice seem to have hearing levels comparable to that of young mice. Additionally, fewer of the critical hearing cells appear to have died in contrast to the so-called wild type mice that did not have the protein deficiency.
In order to examine how resistant the inner ear cells of the Bak-deficient mice were, the researchers were believed to have exposed cells to a chemical that causes oxidative stress. Supposedly, such stress usually induces Bak expression in inner ear cells.
Moreover, there appears to have been only minor loss of cochlear cells at all doses of the stressor chemical as compared to the level observed in wild-type animals. The researchers concluded that Bak may perhaps promote cochlear cell death in response to oxidative stress.
“This paper clearly shows us that oxidative stress causes hearing loss,†says researcher, Jinze Xu, a postdoctoral fellow in Leeuwenburgh’s group.
So if oxidative stress triggers damage and death of hearing-related cells, enhancing the antioxidant defenses of the mitochondria could be able to decrease such damage. The researchers found that both animals, one which had excess amounts of an enzyme that seems to search for reactive oxygen species and those who were fed certain antioxidants orally, beginning of age-related hearing loss was noted to have been delayed.
“It looks like a viable biological target that may be applicable to drug use. The issue is always timing — when to start antioxidant interventions at what combination and what dose,†says Leeuwenburgh.
Huber Warner, associate dean for research a University of Minnesota College of Biological Sciences and former director of the biology of aging program at the National Institute on Aging said that, “This extends research into life extension by caloric restriction into a whole new area that hasn’t been looked at before. The work shows that rather than caloric restriction just having an overall effect on metabolism of nutrients, Bak modulation can have segmental effects on particular physical systems that have age-related problems in humans.â€
Caloric restriction seems to be another way to lessen oxidative damage. Apparently, it has earlier been shown to extend life and prevent age-related hearing loss in the type of mice used in the study.
With the novel findings, the researchers propose that one of the ways that restriction of calories acts may be through reducing the level of cell death that is induced by the protein Bak. The findings of the research could possibly assist in pointing the way toward a novel target for antioxidant therapies.
The findings of the research have been published in the journal, Proceedings of the National Academy of Sciences.