Cargando…

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,...

Descripción completa

Detalles Bibliográficos
Autor principal: Keithley, Elizabeth M.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2019
Materias:
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
_version_ 1783583146038525952
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
work_keys_str_mv AT keithleyelizabethm pathologyandmechanismsofcochlearaging