# No longitudinal association between hearing loss and Alzheimer’s disease pathology

## TL;DR

This study found no link between hearing loss and Alzheimer’s disease pathology over time, suggesting other factors may explain their connection to dementia.

## Contribution

The study provides new evidence against a direct bidirectional relationship between hearing loss and Alzheimer’s disease biomarkers.

## Key findings

- Baseline hearing loss was not linked to changes in p-tau217 or amyloid PET positivity.
- Hearing loss progression did not predict PET outcomes or modify APOE4-related associations.
- Plasma biomarkers were unrelated to longitudinal hearing loss changes.

## 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.

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.