Abstract

Noise‐induced hearing loss (NIHL) and age‐related hearing loss (AHL, or presbycusis) are widespread health problems that will continue to increase as our society ages. NIHL and AHL often coexist in the same ear; however, the conditions under which they interact and the mechanisms by which they do so remain poorly understood. Inspired by epidemiological studies suggesting that noise‐exposed ears age differently from nonexposed ears [Gates et al., ‘‘Logitudinal threshhold changes in people with audiometric notches,’’ Hear. Res. 141, 220–228 (2000)], we studied interactions between NIHL and AHL in mouse; an animal with a short life span, with intrastrain genetic homogeneity to minimize variability and with interstrain differences in vulnerability which can be exploited to probe mechanisms. Using such models, we have uncovered evidence that early noise exposure can have an ongoing influence on the nature and progression of an age‐related hearing loss. The nature of this age‐related hearing loss exacerbation is special; it can occur even in ears without permanent threshold shifts from the noise and leads to massive loss of spiral ganglion neurons despite intact hair cell populations. Findings have practical importance for investigations of NIHL in animal models, and may have implications for clinical practices allocating noise‐induced and age‐related components of hearing loss as strictly additive. [Work supported by NIH.]

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