Illustrative photo of elderly couple.
Researchers in Tel Aviv, New York and Maryland have discovered a protein whose absence causes the loss of hearing in the elderly.
The finding, by researchers at Tel Aviv University and the University of Maryland and just published in the prestigious journal Nature Communications, has been described by experts as a “breakthrough.”
The discovery could lead to the development of treatment for preventing or restoring hearing loss, TAU said.
The decline of hearing in the elderly is becoming more common in the Western world due to the aging of the population and increased exposure to noise. It affects almost half of those aged 70 and over.
Dr. Ronna Hertzano, an assistant professor of otolaryngology and of the head and neck surgery department at the Baltimore university, who received her medical and doctoral degrees at TAU; Dr. Rani Elkon of TAU and Dr. Efrat Eliyahu of Mount Sinai Medical Center in Manhattan worked together on the research.
They discovered that hearing declines in many elderly people due to the loss of cilia (tiny hairs) in the inner ear. Their normal function is dependent on proteins needed for their specific activity, while additional proteins protect them from cell death. Thus, to determine what causes their death, the researchers tried to identify the genes that lead to the production of the proteins.
For this, they isolated various cells from the ears of lab mice and performed a “gene-expression profile” of them. They then managed to identify which genes from the entire mice genome are activated specifically in the cilia. They processed the data and, using bioinformatic analysis, identified the “instructions for activation” of the genes that are expressed only by the ear cilia.
“We compared our findings with the existing database that connect the sequences of DNA letters with the proteins that control gene expression,” the authors explained.
They discovered a clear connection between the cells in the cilia and a known protein called RFX that supervises activity in bodily organs. Its normal functioning is vital for hearing, they continued. The researchers managed to prove their theory in experiments on lab mice, using a model of mice they created genetically that were born without RFX in the ear cilia. At the end of the second week of their lives, when mice begin to hear, the cilia started to die off, making them deaf.
Finally, to characterize the process, cells that were taken from the ears of RFX-less mice were transferred to the Mount Sinai lab where the level of proteins involved in planned cell death (apoptosis) were compared to those that protected their survival. The team now believe their discovery will help develop treatments to restore hearing in patients.
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