Abstract
Most hearing loss results from lesions of the sensory cells and/or neurons of the auditory portion of the inner ear. To date, only the cochlear implantation offers long-term hearing-aid benefit, but still with limited performance and expensive cost. While the underlying causes of deafness are not clear, the death or hair cells and/or neurons and the loss of neuronal contacts are key pathological features. Pinpointing molecular events that control cell death in the cochlea is critical for the development of new strategies to prevent and treat deafness, whether in combination or not with cochlear implant therapy.
Keywords: cochlea, cell death, ototoxicity, noise trauma, neuroprotection, trophic factors
Current Pharmaceutical Design
Title: Molecular Pathways Involved in Apoptotic Cell Death in the Injured Cochlea: Cues to Novel Therapeutic Strategies
Volume: 11 Issue: 17
Author(s): F. Lallemend, P. P. Lefebvre, G. Hans, G. Moonen and B. Malgrange
Affiliation:
Keywords: cochlea, cell death, ototoxicity, noise trauma, neuroprotection, trophic factors
Abstract: Most hearing loss results from lesions of the sensory cells and/or neurons of the auditory portion of the inner ear. To date, only the cochlear implantation offers long-term hearing-aid benefit, but still with limited performance and expensive cost. While the underlying causes of deafness are not clear, the death or hair cells and/or neurons and the loss of neuronal contacts are key pathological features. Pinpointing molecular events that control cell death in the cochlea is critical for the development of new strategies to prevent and treat deafness, whether in combination or not with cochlear implant therapy.
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Cite this article as:
Lallemend F., Lefebvre P. P., Hans G., Moonen G. and Malgrange B., Molecular Pathways Involved in Apoptotic Cell Death in the Injured Cochlea: Cues to Novel Therapeutic Strategies, Current Pharmaceutical Design 2005; 11 (17) . https://dx.doi.org/10.2174/1381612054367346
DOI https://dx.doi.org/10.2174/1381612054367346 |
Print ISSN 1381-6128 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4286 |
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