Think of your ears like a busy city. Noise exposure and aging can cause a decrease in connections between different parts of the city, specifically the auditory nerve fibers and inner hair cells. This connection loss, known as cochlear synaptopathy (CS), may affect how we understand speech. Animal studies have shown that noise exposure leads to more CS than aging alone. Interestingly, older animals may experience either significant or minimal additional synapse loss after noise exposure. In humans, research suggests that both noise and aging can lead to auditory nerve fiber loss. Based on findings from different animal species, we anticipate that noise exposure could speed up age-related CS in humans. Animal studies have linked CS with changes in brainstem response, middle ear reflexes, and the ability to process sound over time. Humans, however, don’t show clear deficits in these measures individually. The combined effects of noise and aging on auditory neural loss in humans are still not well understood and need further investigation. To dig deeper into this fascinating topic, check out the full article!

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.

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