‘Escaped’ proteins add to hearing loss in elderly, UF researchers found
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 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.
“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 called Bak is known to play a role in the weakening of the mitochondrial membrane. The more of the protein present, the leakier the mitochondrial membrane becomes, allowing harmful proteins to travel out into the rest of the cell.
Bak is typically induced by oxidative stress and its levels increase as people age. The researchers wanted to see whether its absence would prevent the 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 were found to have hearing levels comparable to that of young mice. In addition, fewer of the critical hearing cells died, compared with so-called wild type mice that did not have the protein deficiency.
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