Chronic moderate-intensity noise exposure leads to less severe hearing loss but comparable prolonged cognitive impairment compared with acute high-intensity noise exposure.

Noise can induce stress responses and even result in noise-induced hearing loss (NIHL), which is a common form of acquired peripheral hearing loss (HL). Acquired peripheral HL in midlife is the most common modifiable risk factor for dementia, and the underlying mechanism of this relationship deserves more attention due to the increasing prevalence of unsafe listening practices among young people. This study aimed to investigate the effects of different noise exposure paradigms on cognition, hippocampal neurogenesis and hippocampal microglial status, and to analyze the potential roles of stress responses and HL in these effects. Adult C57BL/6 J mice were randomly allocated into a control group or one of two noise groups: Na123 (animals underwent a single 2-h session of acute noise exposure at 123 dB SPL) and Nc100 (animals subjected to chronic noise exposure at 100 dB SPL for 4 h/day for a continuous 28 days). The results revealed a short-term transient stress response after noise exposure in both noise groups with early-stage cognitive impairments observed only in Nc100 mice. Although the Nc100 mice developed less severe HL than the Na123 mice, they exhibited comparable cognitive impairment and hippocampal neurogenesis deficiency accompanied by similar microglial morphological disturbance in the late stage after noise exposure. These findings indicate that both the HL and stress response might collectively and synergistically contribute to the cognitive impairment following noise exposure, and this relationship may be mediated by the hippocampal neurogenesis deficiency and microglial morphological disturbance. Furthermore, these results revealed the detrimental and insidious nature of long-term but moderate-intensity noise exposure.