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The relative and combined effects of noise exposure and aging on auditory peripheral neural deafferentation: A narrative review

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The relative and combined effects of noise exposure and aging on auditory peripheral neural deafferentation: A narrative review. / Shehabi, Adnan; Prendergast, Garreth; Plack, Christopher.
In: Frontiers in Aging Neuroscience, Vol. 14, 877588, 23.06.2022.

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Shehabi A, Prendergast G, Plack C. The relative and combined effects of noise exposure and aging on auditory peripheral neural deafferentation: A narrative review. Frontiers in Aging Neuroscience. 2022 Jun 23;14:877588. doi: 10.3389/fnagi.2022.877588

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@article{6474bdb822b2412c83847a8146e7a653,
title = "The relative and combined effects of noise exposure and aging on auditory peripheral neural deafferentation: A narrative review",
abstract = "Animal studies have shown that noise exposure and aging cause a reduction in the number of synapses between low and medium spontaneous rate auditory nerve fibers and inner hair cells before outer hair cell deterioration. This noise-induced and age-related cochlear synaptopathy (CS) is hypothesized to compromise speech recognition at moderate-to-high suprathreshold levels in humans. This paper evaluates the evidence on the relative and combined effects of noise exposure and aging on CS, in both animals and humans, using histopathological and proxy measures. In animal studies, noise exposure seems to result in a higher proportion of CS (up to 70% synapse loss) compared to aging (up to 48% synapse loss). Following noise exposure, older animals, depending on their species, seem to either exhibit significant or little further synapse loss compared to their younger counterparts. In humans, temporal bone studies suggest a possible age- and noise-related auditory nerve fiber loss. Based on the animal data obtained from different species, we predict that noise exposure may accelerate age-related CS to at least some extent in humans. In animals, noise-induced and age-related CS in separation have been consistently associated with a decreased amplitude of wave 1 of the auditory brainstem response, reduced middle ear muscle reflex strength, and degraded temporal processing as demonstrated by lower amplitudes of the envelope following response. In humans, the individual effects of noise exposure and aging do not seem to translate clearly into deficits in electrophysiological, middle ear muscle reflex, and behavioral measures of CS. Moreover, the evidence on the combined effects of noise exposure and aging on peripheral neural deafferentation in humans using electrophysiological and behavioral measures is even more sparse and inconclusive. Further research is necessary to establish the individual and combined effects of CS in humans using temporal bone, objective, and behavioral measures.",
keywords = "cochlear synaptopathy (CS), noise exposure, age-related hearing loss (ARHL, auditory brainstem response (ABR), summating potential to action potential ratio (SP:AP, envelope-following response (EFR, middle ear muscle reflex (MEMR), speech-perception-in-noise (SPiN)",
author = "Adnan Shehabi and Garreth Prendergast and Christopher Plack",
year = "2022",
month = jun,
day = "23",
doi = "10.3389/fnagi.2022.877588",
language = "English",
volume = "14",
journal = "Frontiers in Aging Neuroscience",
issn = "1663-4365",
publisher = "Frontiers Media S.A.",

}

RIS

TY - JOUR

T1 - The relative and combined effects of noise exposure and aging on auditory peripheral neural deafferentation

T2 - A narrative review

AU - Shehabi, Adnan

AU - Prendergast, Garreth

AU - Plack, Christopher

PY - 2022/6/23

Y1 - 2022/6/23

N2 - Animal studies have shown that noise exposure and aging cause a reduction in the number of synapses between low and medium spontaneous rate auditory nerve fibers and inner hair cells before outer hair cell deterioration. This noise-induced and age-related cochlear synaptopathy (CS) is hypothesized to compromise speech recognition at moderate-to-high suprathreshold levels in humans. This paper evaluates the evidence on the relative and combined effects of noise exposure and aging on CS, in both animals and humans, using histopathological and proxy measures. In animal studies, noise exposure seems to result in a higher proportion of CS (up to 70% synapse loss) compared to aging (up to 48% synapse loss). Following noise exposure, older animals, depending on their species, seem to either exhibit significant or little further synapse loss compared to their younger counterparts. In humans, temporal bone studies suggest a possible age- and noise-related auditory nerve fiber loss. Based on the animal data obtained from different species, we predict that noise exposure may accelerate age-related CS to at least some extent in humans. In animals, noise-induced and age-related CS in separation have been consistently associated with a decreased amplitude of wave 1 of the auditory brainstem response, reduced middle ear muscle reflex strength, and degraded temporal processing as demonstrated by lower amplitudes of the envelope following response. In humans, the individual effects of noise exposure and aging do not seem to translate clearly into deficits in electrophysiological, middle ear muscle reflex, and behavioral measures of CS. Moreover, the evidence on the combined effects of noise exposure and aging on peripheral neural deafferentation in humans using electrophysiological and behavioral measures is even more sparse and inconclusive. Further research is necessary to establish the individual and combined effects of CS in humans using temporal bone, objective, and behavioral measures.

AB - Animal studies have shown that noise exposure and aging cause a reduction in the number of synapses between low and medium spontaneous rate auditory nerve fibers and inner hair cells before outer hair cell deterioration. This noise-induced and age-related cochlear synaptopathy (CS) is hypothesized to compromise speech recognition at moderate-to-high suprathreshold levels in humans. This paper evaluates the evidence on the relative and combined effects of noise exposure and aging on CS, in both animals and humans, using histopathological and proxy measures. In animal studies, noise exposure seems to result in a higher proportion of CS (up to 70% synapse loss) compared to aging (up to 48% synapse loss). Following noise exposure, older animals, depending on their species, seem to either exhibit significant or little further synapse loss compared to their younger counterparts. In humans, temporal bone studies suggest a possible age- and noise-related auditory nerve fiber loss. Based on the animal data obtained from different species, we predict that noise exposure may accelerate age-related CS to at least some extent in humans. In animals, noise-induced and age-related CS in separation have been consistently associated with a decreased amplitude of wave 1 of the auditory brainstem response, reduced middle ear muscle reflex strength, and degraded temporal processing as demonstrated by lower amplitudes of the envelope following response. In humans, the individual effects of noise exposure and aging do not seem to translate clearly into deficits in electrophysiological, middle ear muscle reflex, and behavioral measures of CS. Moreover, the evidence on the combined effects of noise exposure and aging on peripheral neural deafferentation in humans using electrophysiological and behavioral measures is even more sparse and inconclusive. Further research is necessary to establish the individual and combined effects of CS in humans using temporal bone, objective, and behavioral measures.

KW - cochlear synaptopathy (CS)

KW - noise exposure

KW - age-related hearing loss (ARHL

KW - auditory brainstem response (ABR)

KW - summating potential to action potential ratio (SP:AP

KW - envelope-following response (EFR

KW - middle ear muscle reflex (MEMR)

KW - speech-perception-in-noise (SPiN)

U2 - 10.3389/fnagi.2022.877588

DO - 10.3389/fnagi.2022.877588

M3 - Journal article

VL - 14

JO - Frontiers in Aging Neuroscience

JF - Frontiers in Aging Neuroscience

SN - 1663-4365

M1 - 877588

ER -