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Join tens of thousands of doctors, health professionals and patients who receive our newsletters. Researchers from the University of Michigan and Harvard Medical School in Boston, MA, may be well on the way to finding new therapies that restore noise-induced and age-related hearing loss in humans. The researchers, led by Gabriel Corfas, PhD, of the University of Michigan, publish their findings online in the journal eLife.
Approximately 50 million Americans have hearing loss in at least one ear, with around 26 million Americans aged 20-69 experiencing high-frequency hearing loss as a result of noise exposure. In their study, the researchers explain how they were able to increase production of a protein called Neurotrophin-3 (NT3) in mice, which they found plays a key role in communication between the ears and the brain.
In their study, the researchers identified supporting cells in the inner ear that produce NT3. Approximately 2-3 in every 1,000 children in the US are born with detectable levels of hearing loss in one or both ears. For this study, the team used the technique to activate additional NT3 genes that had been introduced to the supporting cells of the inner ear in mice that had been partially deafened by loud noise. The drug tamoxifen was introduced to the supporting cells in the inner ear, which prompted them to produce extra NT3 protein.
The researchers found the mice that had experienced boosted NT3 production regained their hearing over a 2-week period, compared with mice that had not had additional NT3 production. According to the team, these findings indicate that NT3 production is important for making ribbon synapses, and that boosting production of this protein may restore noise-induced and age-related hearing loss. Corfas and his team say they now plan to investigate the role of NT3 in human ears and identify drugs that produce the same effect as the protein, offering the potential to restore hearing loss in humans. The researchers note that the gene therapy technique used in this study has the potential to work in humans, but that a drug-based method would be "simpler" and a drug could be repeatedly administered for as long as it takes for hearing to be restored. The researchers stress, however, that since the mice in this study were only partially deaf, it is unclear whether increased NT3 production would restore hearing in subjects that are fully deaf. Medical News Today recently reported on a study from the University of Leicester in the UK, in which researchers reveal how loud noises damage hearing in more detail.


University of Michigan Health System news release, accessed 21 October 2014 via EurekAlert. Additional source: Hearing Health Foundation, hearing loss and tinnitus statistics, accessed 21 October 2014. Additional source: National Institute on Deafness and Other Communication Disorders, quick statistics, accessed 21 October 2014. Please use one of the following formats to cite this article in your essay, paper or report:MLAWhiteman, Honor. For any corrections of factual information, or to contact our editorial team, please see our contact page.
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Hearing loss is also common as we age, affecting around 30% of adults aged 65-74 and 47% of adults aged 75 and over. The protein is crucial in establishing a super-fast connection between the ear's hair cells and nerve cells - a connection the researchers call the "ribbon synapse." But this ribbon synapse can become damaged as a result of noise exposure or normal aging, which can lead to hearing loss. They set out to see what would happen if they increased production of NT3 through these supporting cells. This allows researchers to activate genes in particular cells by administering a drug that prompts the cells to "read" additional copies of a gene that have been inserted into them.
The researchers then tested the hearing of the mice through a test normally used in humans - the auditory brainstem response (ABR). The researchers say they may offer new strategies to treat neurodegenerative diseases, in which nerve cell connections are impaired. You are seeing this page because a category, product or a page has been deleted from your store.
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