Hearing loss and its link to cognitive impairment and dementia

Abstract

Hearing loss is an important risk factor for the development of dementia, particularly Alzheimer's disease (AD). Mid-life hearing loss increases the risk of developing dementia by double any other single factor. However, given this strong connection between hearing loss and AD, the mechanisms responsible for this link are still unknown. Data from observational studies relating hearing loss and cognitive impairment, measured with standardized questionnaires, has shown a strong relationship between them. Similar findings have emerged from animal studies, showing that the induction of hearing loss via prolonged loud sound exposure or ear canal blocking, can impair cognitive abilities. Interestingly, patients with age-related hearing impairment exhibit increased phosphorylated tau in the cerebrospinal fluid, but no such relationship has been identified for amyloid-β. In addition, hearing loss predisposes to social isolation precipitating the development of dementia through a supposed reduction in cognitive load and processing requirements. Given this link between hearing loss and dementia, the question arises whether the restoration of hearing might mitigate against the onset or progress of AD. Indeed, there is a growing body of research that suggests that those who wear hearing aids for age-related hearing problems maintain better cognitive function over time than those who do not. These are compelling findings, as they suggest the use of hearing aids has the potential to be a cost-effective treatment for those with hearing loss both prior (for those at high risk for AD) and after the development of symptoms. This review aims to summarize the current theories that relate hearing loss and cognitive decline, present the key findings of animal studies, observational studies and summarize the gaps and limitations that need to be addressed in this topic. Through this, we suggest directions for future studies to tackle the lack of adequately randomized control trials in the field. This omission is responsible for the inability to provide a conclusive verdict on whether to use hearing interventions to target hearing-loss related cognitive decline.

Keywords: Alzheimer's disease; cochlear implant; cognitive impairment; dementia; hearing aid; hearing loss; models of hearing loss.

Figure 1

Different types of age-related hearing impairment, including atrophy of the stria vascularis, hair cell loss and primary cochlear neuron degeneration (Quaranta et al., ; Fortunato et al., 2016). Specific changes seen in stria vascularis include age-related morphological changes such as numerous cytoplasmic vacuoles, enlargement of intracellular spaces and irregularity of mitochondria and its constituents, most notably disorganization of cristae (Lyu et al., 2020). These changes have been shown to be precipitated by oxidative damage and downregulation of TMEM16A, a calcium-activated chloride channel (Spicer and Schulte, ; Zhou et al., 2019). Cochlear disease or trauma have been shown to give rise to hair cell loss, with potential causative factors including continuous industrial noise exposure, reactive oxygen species and Superoxide dismutase (SOD1) deficiency (McFadden et al., ,, ; Emmerich et al., ; Huang et al., ; Vlajkovic and Thorne, 2021). Primary neural degeneration via disconnecting of auditory neurones from their hair cell targets during aging has been shown to trigger the loss of hair cells (Viana et al., ; Wu et al., 2019). Studies have identified that loss of GABA in the central nucleus of the inferior colliculus and the build-up of reactive oxygen species has led to neural presbycusis (Caspary et al., , ; Huang et al., 2000). Made using BioRender software. CAP, central auditory processing; ROS, reactive oxygen species.