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Using gene therapy, researchers at Boston Children's Hospital and Harvard Medical School have restored hearing in mice with a genetic form of deafness. The other type of mouse, called Beethoven, has a specific TMC1 mutationa€”a change in a single amino acida€”and is a good model for the dominant form of TMC1-related deafness. To deliver the healthy gene, the team inserted it into an engineered virus called adeno-associated virus 1, or AAV1, together with a promotera€”a genetic sequence that turns the gene on only in certain sensory cells of the inner ear known as hair cells. In the recessive deafness model, gene therapy with TMC1 restored the ability of sensory hair cells to respond to sounda€”producing a measurable electrical currenta€”and also restored activity in the auditory portion of the brainstem. A scanning electron microscope image zooming into the v-shaped sensory hair bundles in the cochlea. AAV1 is considered safe as a viral vector and is already in use in human gene therapy trials for blindness, heart disease, muscular dystrophy and other conditions. Ultimately, Holt hopes to partner with clinicians at Boston Children's Department of Otolaryngology and elsewhere to start clinical trials of TMC1 gene therapy within 5 to 10 years. Holt believes that other forms of genetic deafness may also be amenable to the same gene therapy strategy.
Holt's team showed in 2013 that TMC1 and the related protein TMC2 are critical for hearing, ending a rigorous 30-year search by scientists. Although the channel is made up of either TMC1 or TMC2, a mutation in the TMC1 gene is sufficient to cause deafness. A new gene therapy approach can reverse hearing loss caused by a genetic defect in a mouse model of congenital deafness, according to a preclinical study published by Cell Press in the July 26 issue of the journal Neuron. A specific protein found in the bridge-like structures that make up part of the auditory machinery of the inner ear is essential for hearing.

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This journal is a member of and subscribes to the principles of the Committee on Publication Ethics. Their work, published online July 8 by the journal Science Translational Medicine, could pave the way for gene therapy in people with hearing loss caused by genetic mutations.
Kirby Neurobiology Center at Boston Children's and an associate professor of Otolaryngology at Harvard Medical School.
One type had the TMC1 gene completely deleted, and is a good model for recessive TMC1 mutations in humans: Children with two mutant copies of TMC1 have profound hearing loss from a very young age, usually by around 2 years. In this form, less common than the recessive form, a single copy of the mutation causes children to gradually go deaf beginning around the age of 10 to 15 years. The researchers screened various types of AAV and various types of promoters to choose the best-performing combination. Overall, severe to profound hearing loss in both ears affects 1 to 3 per 1,000 live births. When sound vibrations strike the bundle, the hairs, or microvilli, wiggle back and forth, opening and closing channels formed by TMC proteins.

Sensory hair cells in the inner ear contain tiny projections called microvilli, each with a channel at its tip formed by TMC1 and TMC2 proteins.
However, Holt's study also showed that gene therapy with TMC2 could compensate for loss of a functional TMC1 gene, restoring hearing in the recessive deafness model and partial hearing in the dominant deafness model. Researchers have found a new health benefit of resveratrol, which occurs naturally in blueberries, raspberries, mulberries, grape skins and consequently in red wine.
They chose TMC1 because it is a common cause of genetic deafness, accounting for 4 to 8 percent of cases, and encodes a protein that plays a central role in hearing, helping convert sound into electrical signals that travel to the brain.
To test hearing, the researchers placed the mice in a "startle box" and sounded abrupt, loud tones.
They plan to further optimize their protocol and follow their treated mice to see if they retain hearing longer than the two months already observed. When open, the channels allow calcium into the cell, initiating electrical signals that travel to the brain.
When sound waves wash over the microvilli, they wiggle and the mechanical stimulation causes the channel to open.
This allows calcium to enter the cell, generating an electrical signal that travels to the brain and ultimately translates to hearing. And if I do I'll rule the world someday and crush all the people who give my posts lousy scores.

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