No longitudinal association between hearing loss and Alzheimer’s disease pathology
Year: 2026
Type: article
Study design: Observational Study
Abstract: • Baseline hearing loss (HL) was not linked to longitudinal changes in p-tau217. • Baseline HL was not associated with incident amyloid PET positivity. • HL progression did not predict PET outcomes. • APOE4 carriership did not modify associations with Aβ PET. • Baseline plasma biomarkers were also unrelated to longitudinal HL changes. Hearing loss (HL) is a potential risk factor for Alzheimer’s disease (AD), with animal studies suggesting a bidirectional relationship. This study examines whether HL links to changes in AD pathology and, whether AD biomarkers relate to subsequent HL progression. Baseline Aβ42/Aβ40 and p-tau217 were measured using single-molecule arrays in 474 participants of the Rotterdam Study (mean age=62.37) between 2010-2016. HL was defined as the better-ear’s pure-tone threshold average. After seven years, participants underwent amyloid PET; HL and p-tau217 were reassessed two years after PET. Baseline HL was not associated with amyloid PET positivity, Aβ42/Aβ40, or longitudinally with p-tau217. Likewise, HL progression did not predict PET outcomes. APOE4 carriership did not modify associations with Aβ PET. Similarly, baseline plasma biomarkers were also unrelated to longitudinal HL changes. No bidirectional association was observed between HL and AD pathology, suggesting that HL may contribute to dementia through other pathways.
Institutions: Erasmus MC, Erasmus University Rotterdam
Language: English
Subfield: Psychiatry and Mental health
Field: Medicine
Domain: Health Sciences
Open Access status: gold
Estimated APC paid: $4,060
Awards: G1613806636, G1798618210, G2501976640, G3927062555, Exploit population imaging to unravel resistance to Alzheimer's disease, G434337789, Exploit population imaging to unravel resistance to Alzheimer's disease, G5616778589, G7108286715, Amyloid and vascular pathology: a tale of two pathways, G975443604
OpenAlex ID: W7125001569
