Abstract
Sensorineural hearing loss (SNHL) is a common disability in the world; however, at present, options for the pharmacological treatment of SNHL are very limited. Previous studies involving human temporal bone analyses have revealed that the degeneration of the cochlea is a common mechanism of SNHL. A major problem for the development of novel pharmacotherapy for SNHL has been the limited regeneration capacity in mammalian cochlear cells. However, recent progress in basic studies has led to several effective strategies for the induction of regeneration in the mammalian cochlea, in accordance with the stage of degeneration. In addition, recent advances in the identification of human deafness genes and their characterization in mouse models have elucidated cellular and/or molecular mechanisms of SNHL, which will contribute to clarify molecular targets of pharmacotherapy for treatment of SNHL.
Highlights
Hearing impairment has been the most common cause of disability worldwide
Hearing impairment can be subdivided into two types, conductive and sensorineural hearing loss (SNHL)
Conductive hearing loss is largely overcome by surgical treatment, therapeutic options for SNHL are limited to hearing aids and cochlear implants, if the hearing loss has been reversed
Summary
Hearing impairment has been the most common cause of disability worldwide. Hearing impairment can be subdivided into two types, conductive and sensorineural hearing loss (SNHL). Beside hair cells and spiral ganglion neurons, there are a number of other cochlear components that are included in a list of possible therapeutic targets. Many studies have been focused on morphological findings in human temporal bones, i.e., the following four classical types of SNHL etiology: the loss of hair cells, loss of spiral ganglion neurons, degeneration of the stria vascularis, and combinations (Merchant and Nadol, 2010).
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