The Relative Contribution of Cochlear Synaptopathy and Reduced Inhibition to Age-Related Hearing Impairment for People With Normal Audiograms

Abstract

Older people often show auditory temporal processing deficits and speech-in-noise intelligibility difficulties even when their audiogram is clinically normal. The causes of such problems remain unclear. Some studies have suggested that for people with normal audiograms, age-related hearing impairments may be due to a cognitive decline, while others have suggested that they may be caused by cochlear synaptopathy. Here, we explore an alternative hypothesis, namely that age-related hearing deficits are associated with decreased inhibition. For human adults (N = 30) selected to cover a reasonably wide age range (25–59 years), with normal audiograms and normal cognitive function, we measured speech reception thresholds in noise (SRTNs) for disyllabic words, gap detection thresholds (GDTs), and frequency modulation detection thresholds (FMDTs). We also measured the rate of growth (slope) of auditory brainstem response wave-I amplitude with increasing level as an indirect indicator of cochlear synaptopathy, and the interference inhibition score in the Stroop color and word test (SCWT) as a proxy for inhibition. As expected, performance in the auditory tasks worsened (SRTNs, GDTs, and FMDTs increased), and wave-I slope and SCWT inhibition scores decreased with ageing. Importantly, SRTNs, GDTs, and FMDTs were not related to wave-I slope but worsened with decreasing SCWT inhibition. Furthermore, after partialling out the effect of SCWT inhibition, age was no longer related to SRTNs or GDTs and became less strongly related to FMDTs. Altogether, results suggest that for people with normal audiograms, age-related deficits in auditory temporal processing and speech-in-noise intelligibility are mediated by decreased inhibition rather than cochlear synaptopathy.

Quantifying the Impact of Auditory Deafferentation on Speech Perception

“…This loss is much smaller than what our model and behavioral results suggest is needed for synaptopathy or deafferentation to affect speech intelligibility in noise. This could therefore explain why some authors have reported that even though synaptopathy occurs naturally with aging, it is not sufficient to affect speech-in-noise perception ( Bramhall et al, 2019 ; Gómez-Álvarez et al, 2023 ; Johannesen et al, 2019 ).…”

Effects of Age and Noise Exposure History on Auditory Nerve Response Amplitudes: A Systematic Review, Study, and Meta-Analysis

“…The large number of studies returned by these search queries (1,278 ABR, 223 CAP) were checked by three experts (authors Dias, Harris, and McClaskey) to confirm they matched our search criteria and further filtered to include only those studies that measured ABR WI or CAP N1 response amplitude and explicitly tested and reported the relationship between ABR WI or CAP N1 response amplitude and age or noise exposure. As a consequence, some studies that motivated our study were excluded from one or both meta-analyses for reporting the relationships of other metrics of AN function instead of ABR WI/CAP N1 response amplitude (e.g., Gómez-Álvarez et al, 2023;Johannesen et al, 2019) or for not providing descriptive or inferential statistics needed to calculate the effect size of the relationship between ABR WI/CAP N1 response amplitude and age or noise exposure history, typically for non-significant relationships (e.g., Maele et al, 2021;Megha et al, 2021;Prendergast et al, 2019;Ripley et al, 2022). The latter is important to consider because the mean effect size computed across studies may be biased by significant effects reported within published studies, providing an inflated mean effect size that is larger than the true population mean (Cumming, 2012;Rosenthal, 1991).…”

Cochlear Ribbon Synapses in Aged Gerbils

“…Currently, there is intriguing evidence for preferential, disproportionate loss in the low-SR population [ 13 , 20 , 21 , 22 , 23 , 24 , 25 ]. However, perceptual deficits that may arise from this have been difficult to identify in humans and remain controversial [ 26 , 27 , 28 , 29 ]. Animal studies that aim to directly correlate cochlear synaptopathy and physiology or perception remain rare and have yielded mixed results [ 13 , 30 ].…”