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Published on: June 25, 2019
Regional brain atrophy mediates age effects on words recognition in noise in adults
Samin Ashjaei1, Julius Fridriksson2, Leonardo Bonilha3
1Department of Communication Sciences and Disorders, University of South Carolina, Close-Hipp Building, Room 268, 1705 College Street, Columbia 29208, SC, USA.
Abstract:
Aging in adults is associated with a decline in speech-in-noise (SiN) recognition, yet the neural mechanisms driving this decline remain insufficiently characterized. Most neural evidence on age-related SiN performance has relied on correlational approaches that describe how SiN ability is related to age, but it is not yet clear how changes in specific brain structures mediate this relationship. Moreover, it remains unclear how such mediation manifests when hearing sensitivity is clinically normal. The present study applied a brain-wide, region-level mediation framework to identify the neural pathways through which regional brain atrophy mediates age effects on SiN performance. We studied data from 208 adults (aged 20-80 years; M = 49.5, SD = 19.6) who participated in the Aging Brain Cohort (ABC) Study at the University of South Carolina. Participants completed pure-tone audiometry (PTA) test, the Words-in-Noise (WIN) test, and underwent high-resolution structural MRI. Regional gray- and white-matter volumes were derived using the Johns Hopkins University atlas, and mediation was assessed using the graphical Brain Association Tool (gBAT) to systematically examine how reduced brain volume mediates age-WIN recognition link. A secondary analysis examined mediation effects in a subgroup of 150 participants with clinically normal hearing sensitivity. Behavioral results showed that each additional decade of life was associated with approximately 1.3 dB SNR increase in WIN thresholds. Whole-brain mediation analyses showed that age-related atrophy in regions supporting selective attention, error monitoring, working memory, motor control, and multimodal cue integration mediated age-associated declines in SiN recognition. These neural mediation effects persisted, though with reduced magnitude, in the subgroup with clinically normal hearing sensitivity. The results identify brain structural mechanisms underlying SiN difficulties and emphasize that age-related changes in brain structure impair SiN performance even when audibility remains intact.
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