Age-related hearing loss in older adults: etiology and rehabilitation strategies

Abstract

Age-related hearing loss (ARHL) is a prevalent sensory organ disorder among elderly individuals that significantly impacts their cognitive function, psychological well-being, and ability to perform activities of daily living. As the population ages, the number of ARHL patients is increasing. However, the Audiological rehabilitation (AR) status of patients is not promising. In recent years, there has been an increasing focus on the health and rehabilitation of elderly individuals, and significant progress has been made in researching various age-related disorders. However, a unified definition of ARHL in terms of etiology and rehabilitation treatment is still lacking. This study aims to provide a reference for future research on ARHL and the development of AR strategies by reviewing the classification, etiology, and rehabilitation of ARHL.

Keywords: age-related hearing loss; elderly; presbycusis; rehabilitation; review.

Figure 1

Major histopathologic changes in patients with ARHL and corresponding rehabilitation strategies. Histopathologic changes in patients with ARHL are found mainly in the middle ear (tympanic membrane, tympanic chamber), inner ear (cochlea, auditory nerve), and central nervous system, and different types of pathologic changes lend themselves to different rehabilitation strategies. By Biorender.

Figure 2

Reduced Na/K-ATPase activity leads to accelerated cochlear aging. In aging CBA/Caj mice, Na/K-ATPase activity is reduced by approximately 80%. This change impedes cochlear hair cell movement, synaptic activity, and auditory neuron firing, accelerating the aging of these energy-demanding tissues. By Figdraw.

Figure 3

Inflammatory response may be one of the pathogenic mechanisms of ARHL. SAMP8 mice exhibited immune factor recruitment both at aging and in noise-exposed mice. Cellular experiments demonstrated that ROS induced cochlear cells to produce inflammatory vesicles, which regulated caspase-1-dependent activation of IL-1β and IL-18. By Figdraw.

Figure 4

ROS accelerate cochlear cell senescence by damaging cell membrane lipids and DNA. Upon ROS damage, guanines in DNA are susceptible to 8-oxoG production, which leads to telomere fragility, localized DDR signaling, and MiDAS repair, thereby activating p53 to promote cellular senescence. ROS can cause lipid peroxidation of cell membranes, resulting in the production of MDA and 4-HNE, and MDA can cause secondary oxidative damage to proteins. By Figdraw.