Abstract
Several studies identified hearing loss as a risk factor for aging-related processes, including neurodegenerative diseases, as dementia and age-related hearing loss (ARHL). Although the association between hearing impairment in midlife and ARHL has been widely documented by epidemiological and experimental studies, the molecular mechanisms underlying this association are not fully understood. In this study, we used an established animal model of ARHL (C57BL/6 mice) to evaluate if early noise-induced hearing loss (NIHL) could affect the onset or progression of age-related cochlear dysfunction. We found that hearing loss can exacerbate ARHL, damaging sensory-neural cochlear epithelium and causing synaptopathy. Moreover, we studied common pathological markers shared between hearing loss and ARHL, demonstrating that noise exposure can worsen/accelerate redox status imbalance [increase of reactive oxygen species (ROS) production, lipid peroxidation, and dysregulation of endogenous antioxidant response] and vascular dysfunction [increased expression of hypoxia-inducible factor-1alpha (HIF-1α) and vascular endothelial growth factor C (VEGFC)] in the cochlea. Unveiling the molecular mechanisms underlying the link between hearing loss and aging processes could be valuable to identify effective therapeutic strategies to limit the effect of environmental risk factors on age-related diseases.
Highlights
Noise exposure and aging, either independently or synergistically, have long been associated with the development of hearing loss in the adult/elderly population [World Health Organization [WHO], 2006; Liberman, 2017; Kujawa and Liberman, 2019]
In order to evaluate if noise exposure could accelerate or exacerbate age-related hearing loss (ARHL), we exposed 2 M animals to an acoustic trauma and we analyzed auditory threshold at different times to monitor the progression of hearing loss
One month after noise exposure, a threshold elevation of about 50 dB across mid and high frequencies was recorded in NE group, compared with age-matched NN group (Figure 2B), and no differences were present at low frequencies
Summary
Either independently or synergistically, have long been associated with the development of hearing loss in the adult/elderly population [World Health Organization [WHO], 2006; Liberman, 2017; Kujawa and Liberman, 2019]. To identify the coincident, overlapping, or independent mechanisms shared by noise and age-induced cochlear damage becomes critical for hearing loss treatment and prevention (Huang and Tang, 2010; Alvarado et al, 2019; Kujawa and Liberman, 2019) Several factors such as accumulated oxidative damage caused by reactive oxygen species (ROS) production, mitochondrial dysfunction in the cochlea due to increased metabolic activity after noise overstimulation, metabolism dysregulation associated with age, and an impaired homeostasis of cochlear blood supply could play a role in the etiopathogenesis of both NIHL and ARHL [Mills and Schmiedt, 2004; Bielefeld et al, 2010; Huang and Tang, 2010; Fetoni et al, 2011; Alvarado et al, 2015; World Health Organization [WHO], 2018]. Substantiating such correlation between hearing loss and cochlear aging processes would have significant implications for prevention and treatment
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