GAINESVILLE, Fla. Age-related hearing loss is the most common sensory disorder among the elderly. But scientists are still trying to figure out what cellular processes govern or contribute to the loss.
Now a University of Florida team and researchers from University of Wisconsin and three other institutions have identified a protein that is central to processes that cause oxidative damage to cells and lead to age-related hearing loss.
The findings help point the way toward a new target for antioxidant therapies and will be published online this week in the Proceedings of the National Academy of Sciences.
One theory of aging holds that free radicals damage components of mitochondria, the energy center of cells. Such damage accumulates over time, leading to a destabilization of the mitochondria, which leads to release of certain proteins.
"Within the mitochondria these proteins cause life, but when they're out they're deadly," professor Christiaan Leeuwenburgh, Ph.D., chief of the biology of aging division at UF's College of Medicine and a member of the Institute on Aging.
The cell death triggered by the escaped proteins lead to physical effects we associate with aging, such as hearing loss.
More than 40 percent of people in the United States older than 65 suffer from age-related hearing loss, according to data from the National Health Survey. 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," said Shinichi Someya, first author of the paper and a postdoctoral fellow in the group of Tomas Prolla of University of Wisconsin.
Age-related hearing loss involves the death of certain sensory hair, nerve and membrane cells in the inner ear. Since the hair and nerve cells do not regenerate in humans, their death leads to permanent hearing loss.
One protein c
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