Hearing impairment and dementia: cause, catalyst or consequence?

Abstract

The relationship between hearing impairment and dementia has attracted significant attention, the 2024 Lancet Commission report identifying hearing loss as the largest modifiable risk factor for dementia from mid-life. The nature of this linkage between dementia and hearing remains unclear and is likely to be complex. In principle, hearing impairment could cause (directly promote), catalyze (amplify) or be a consequence of neurodegenerative pathology and cognitive decline. Here we use this framework to examine different lines of evidence for the association between hearing impairment and dementia, and consider how this evidence speaks to potential mechanisms and treatment implications. We conclude by considering practical clinical implications for management of patients with hearing impairment and dementia, the potential role for central hearing tests as 'auditory biomarkers' of dementia, and the need for further collaborative and mechanistically motivated research in this area.

Keywords: Alzheimer’s disease; Auditory; Biomarkers; Dementia; Frontotemporal dementia; Hearing.

Fig. 1

Summary of candidate mechanisms by which hearing impairment might be linked to cognitive decline in dementia. A Schematic showing the directionality of candidate effects – hearing loss might directly promote neurodegenerative brain pathology (CAUSE), result from neurodegenerative pathology (CONSEQUENCE) or promote other factors (e.g., impaired communication, reduced cognitive reserve) that themselves exacerbate cognitive decline and thereby amplify the effects of underlying neurodegenerative pathology (CATALYST). The cause and catalysis mechanisms relate to peripheral hearing impairment and the consequence mechanism to central hearing (in this context, auditory cognitive) impairment, though these can be difficult to distinguish clinically (see text). B Panels schematising how these candidate mechanisms might affect the detection of clinical cognitive decline, and the potential impact of hearing aids. Over time (x axis), evolution of neurodegenerative brain pathology (y axis) eventually attains a threshold level (horizontal gray line) for the emergence of cognitive dysfunction sufficient for a clinical diagnosis of dementia (DEMENTIA DEVELOPMENT, panel 1). If hearing impairment accelerates neurodegenerative brain pathology (CAUSE, panel 2) this will also tend to accelerate the emergence of clinical dementia ( compare red solid oblique line [hearing loss] in panel 2 vs black solid oblique line [no hearing loss] in panel 1). If hearing impairment amplifies the clinical effects of underlying neurodegenerative pathology (CATALYST, panel 3) this will tend to make clinical dementia (as diagnosed using currently standard cognitive tests) detectable at a lower level of underlying neurodegenerative brain pathology (compare the horizontal grey lines in panel 3 [hearing loss] and panel 1 [no hearing loss]) . If hearing impairment is an early result of underlying neurodegenerative brain pathology (CONSEQUENCE, panel 4) this may be detectable using tests that assess auditory cognition before cognitive decline becomes evident on standard cognitive tests (panel 4, shaded blue area). Dashed lines (panels 2 and 3) indicate the potential impact of hearing aids on the neurodegenerative process and/or emergence of clinical dementia in each scenario; standard amplification-based hearing aids are not anticipated to substantially benefit auditory brain dysfunction (panel 4). C These mechanisms are not mutually exclusive and their effects are likely to interact in the individual patient, their relative importance varying over time and with proximity to clinical dementia onset (time courses of effects coded here as overlapping arrows). Midlife hearing loss promoting pathogenic protein deposition and spread would alter the overall preclinical trajectory of neurodegenerative disease (a process potentially extending over decades, and indicated here schematically rather than to scale; effects on proteinopathy, red arrow). Auditory brain dysfunction resulting from evolving neurodegenerative pathology would produce deficits on tests of auditory cognition, potentially as an early signal of proximity to clinical dementia onset as well as in established dementia (effects on auditory cognition, blue arrow); while the amplifying effects of reduced auditory input on cognitive decline would also begin to act before clinical dementia onset but advance the onset of clinical dementia (catalytic effects, green arrow). Note that the sequence of catalytic and auditory cognitive effects shown here is speculative; catalytic effects could potentially lead auditory cognitive effects. However, all three mechanisms may be operating (and interacting synergistically) around the time of dementia onset