Speech-in-Noise Ability and Longitudinal Cortical Thinning in Speech-Processing Networks

Age-related hearing loss is a major modifiable risk factor for dementia, yet the neural mechanisms linking auditory dysfunction to brain aging and cognitive decline remain unclear. In particular, it is unknown whether peripheral hearing loss, central auditory processing deficits, or hearing aid use best predict neurodegenerative change in older adults.

To determine whether hearing thresholds, speech-in-noise ability, and hearing aid use are associated with longitudinal cortical atrophy and cognitive trajectories in cognitively normal older adults.

This population-based, longitudinal cohort study with baseline and 3-year follow-up assessments was conducted among community-dwelling older adults in Australia. Participants were selected from the Aspirin in Reducing Events in the Elderly trial and categorized as having normal hearing, unaided hearing loss, or using hearing aids based on audiometry and self-reported hearing aid use. Structural magnetic resonance imaging, auditory, and cognitive data were collected between 2012 and 2017. Data were analyzed from August to October 2025.

Peripheral hearing loss assessed using better-ear 4-frequency average thresholds, central auditory processing assessed using binaural speech-in-noise performance, and hearing aid use and duration of use.

Longitudinal change in cortical thickness and regional brain volumes derived from T1-weighted magnetic resonance imaging, focusing on auditory and Alzheimer disease-vulnerable regions. Global cognition was assessed using the Modified Mini-Mental State Examination.

A total of 312 adults (mean [SD] age, 73.5 [3.3] years; 167 [54%] female) without dementia at baseline were included. At baseline, hearing loss groups showed poorer audiometric and speech-in-noise performance but did not differ in global cognition. Over 3 years, widespread age-related cortical atrophy was observed, and poorer baseline speech-in-noise performance was associated with faster cortical thinning in inferior parietal (β = -0.002; 95% CI, -0.003 to 0.001), precuneus (β = -0.001; 95% CI, -0.002 to 0.000), middle temporal cortex (β = -0.001; 95% CI, -0.002 to -0.001), and superior temporal sulcus regions (β = -0.001; 95% CI, -0.002 to 0.000), independent of hearing thresholds and hearing aid use. There was not a statistically significant association between hearing loss/hearing aid use and longitudinal neurostructural change or cognitive decline.

In this cohort study of cognitively normal older adults, central auditory processing impairment, not peripheral hearing loss or hearing aid use, was associated with accelerated cortical thinning in speech-processing networks. Speech-in-noise performance may represent an early behavioral marker of neural vulnerability preceding measurable cognitive decline.