Hearing Loss as a Potentially Modifiable Marker of Dementia Risk: Neurological Evidence, Uncertainty, and Clinical Interpretation

Hearing impairment has emerged as a consistently associated and potentially modifiable risk factor for cognitive decline and dementia, including Alzheimer’s disease (AD). Epidemiological studies demonstrate an increased dementia risk among individuals with hearing loss, with evidence of dose–response relationships across levels of auditory decline. Despite the robustness of this association, the mechanisms linking auditory dysfunction to cognitive deterioration remain multifactorial and incompletely understood. Current evidence points to several interacting pathways, including sensory deprivation and cortical reorganization, increased cognitive load during effortful listening, psychosocial consequences such as social isolation and depression, and potentially overlapping neurobiological processes. Emerging research further suggests that central auditory processing deficits may represent early functional markers of cortical vulnerability associated with neurodegeneration. Clinically, these insights emphasize the importance of routine hearing assessment in older adults and highlight observational evidence indicating that hearing rehabilitation, particularly hearing aid use, may be associated with more favorable cognitive outcomes, although causal effects have yet to be established. By integrating biological, cognitive, and psychosocial perspectives while explicitly addressing persistent uncertainties, this critical narrative review provides a balanced framework for interpreting the relationship between hearing impairment and AD and discusses its implications for prevention and clinical practice. Overall, hearing loss should be regarded as a robustly associated and potentially modifiable marker of dementia risk rather than a confirmed causal determinant. From a neurological standpoint, central auditory dysfunction may therefore reflect underlying brain vulnerability in aging rather than act as a direct causal driver of Alzheimer’s disease.