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Pathology and mechanisms of cochlear aging
Presbycusis, or age‐related hearing loss (ARHL), occurs in most mammals with variations in the age of onset, rate of decline, and magnitude of degeneration in the central nervous system and inner ear. The affected cochlear structures include the stria vascularis and its vasculature, spiral ligament,...
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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John Wiley and Sons Inc.
2019
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7496655/ https://www.ncbi.nlm.nih.gov/pubmed/31066107 http://dx.doi.org/10.1002/jnr.24439 |
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author | Keithley, Elizabeth M. |
author_facet | Keithley, Elizabeth M. |
author_sort | Keithley, Elizabeth M. |
collection | PubMed |
description | Presbycusis, or age‐related hearing loss (ARHL), occurs in most mammals with variations in the age of onset, rate of decline, and magnitude of degeneration in the central nervous system and inner ear. The affected cochlear structures include the stria vascularis and its vasculature, spiral ligament, sensory hair cells and auditory neurons. Dysfunction of the stria vascularis results in a reduced endocochlear potential. Without this potential, the cochlear amplification provided by the electro‐motility of the outer hair cells is insufficient, and a high‐frequency hearing‐loss results. Degeneration of the sensory cells, especially the outer hair cells also leads to hearing loss due to lack of amplification. Neuronal degeneration, another hallmark of ARHL, most likely underlies difficulties with speech discrimination, especially in noisy environments. Noise exposure is a major cause of ARHL. It is well‐known to cause sensory cell degeneration, especially the outer hair cells at the high frequency end of the cochlea. Even loud, but not uncomfortable, sound levels can lead to synaptopathy and ultimately neuronal degeneration. Even in the absence of a noisy environment, aged cells degenerate. This pathology most likely results from damage to mitochondria and contributes to degenerative changes in the stria vascularis, hair cells, and neurons. The genetic underpinnings of ARHL are still unknown and most likely involve various combinations of genes. At present, the only effective strategy for reducing ARHL is prevention of noise exposure. If future strategies can improve mitochondrial activity and reduce oxidative damage in old age, these should also bring relief. |
format | Online Article Text |
id | pubmed-7496655 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-74966552020-09-25 Pathology and mechanisms of cochlear aging Keithley, Elizabeth M. J Neurosci Res Minireviews Presbycusis, or age‐related hearing loss (ARHL), occurs in most mammals with variations in the age of onset, rate of decline, and magnitude of degeneration in the central nervous system and inner ear. The affected cochlear structures include the stria vascularis and its vasculature, spiral ligament, sensory hair cells and auditory neurons. Dysfunction of the stria vascularis results in a reduced endocochlear potential. Without this potential, the cochlear amplification provided by the electro‐motility of the outer hair cells is insufficient, and a high‐frequency hearing‐loss results. Degeneration of the sensory cells, especially the outer hair cells also leads to hearing loss due to lack of amplification. Neuronal degeneration, another hallmark of ARHL, most likely underlies difficulties with speech discrimination, especially in noisy environments. Noise exposure is a major cause of ARHL. It is well‐known to cause sensory cell degeneration, especially the outer hair cells at the high frequency end of the cochlea. Even loud, but not uncomfortable, sound levels can lead to synaptopathy and ultimately neuronal degeneration. Even in the absence of a noisy environment, aged cells degenerate. This pathology most likely results from damage to mitochondria and contributes to degenerative changes in the stria vascularis, hair cells, and neurons. The genetic underpinnings of ARHL are still unknown and most likely involve various combinations of genes. At present, the only effective strategy for reducing ARHL is prevention of noise exposure. If future strategies can improve mitochondrial activity and reduce oxidative damage in old age, these should also bring relief. John Wiley and Sons Inc. 2019-05-07 2020-09 /pmc/articles/PMC7496655/ /pubmed/31066107 http://dx.doi.org/10.1002/jnr.24439 Text en © 2019 The Authors. Journal of Neuroscience Research Published by Wiley Periodicals, Inc. This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Minireviews Keithley, Elizabeth M. Pathology and mechanisms of cochlear aging |
title | Pathology and mechanisms of cochlear aging |
title_full | Pathology and mechanisms of cochlear aging |
title_fullStr | Pathology and mechanisms of cochlear aging |
title_full_unstemmed | Pathology and mechanisms of cochlear aging |
title_short | Pathology and mechanisms of cochlear aging |
title_sort | pathology and mechanisms of cochlear aging |
topic | Minireviews |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7496655/ https://www.ncbi.nlm.nih.gov/pubmed/31066107 http://dx.doi.org/10.1002/jnr.24439 |
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