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Projects

Molecular Mechanisms in Cochlear Regeneration

Molecular Mechanisms in Cochlear RegenerationWe are seeking a graduate student for this NIH-funded project.
Why don’t mammals regenerate dying auditory cells? What signals can stimulate cochlear supporting cell proliferation, and what signals stimulate hair cell differentiation? More importantly, if it is possible to stimulate these actions in cochlear cells, why don’t they occur after mammals are deafened? Are the signals not present, or are they blocked somehow?

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Hearing Restoration

ear imageWe are seeking a graduate student for this UR Ventures-funded project. 
Preliminary data indicates that the activation of ERBB2/3 signaling after noise damage can promote hearing restoration in mice (preprint article).  Translation of this discovery into a solution for hearing loss has already begun.  In collaboration with Prof. Danielle Benoit, we are testing formulations of biomaterials to drive the activation of ERBB2/3 signaling in cochlear supporting cells.  These materials are delivered to the mouse cochlea using a minor surgical procedure.  Preliminary data indicates that they diffuse throughout the cochlea and can be taken up by supporting cells.  Further efforts are needed to assess their efficacy and to find ways to improve the restorative response.

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Genetic Mechanisms in Susceptibility to Noise Damage

Foxo3 expressed in cochleaThere is a wide variation in individual susceptibility to noise damage among workers experiencing a similar acoustic environment. Some of this variation can be attributed to differences in genes. We are interested in identifying genes that are necessary to restore cochlear function after noise damage. Our ultimate goal is to understand how noise damages cochlear cells, driving death and dysfunction, as a necessary first step in hearing restoration.

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Hearing Loss Comorbidities

Hearing Loss ComorbiditiesCaring for patients with Alzheimer’s Disease (AD) costs $250 billion dollars every year in the United States, and as such any interventions that might slow its onset would have great value to society. Strikingly, untreated hearing loss in middle age is comorbid with AD at older ages.  The reasons why hearing loss might presage AD are not understood.

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