The findings suggest that poor speech-in-noise hearing may be an early marker of underlying dementia processes.
Willa Brenowitz, PhD, MPH
Carrying a genetic risk for Alzheimer disease (AD) influences speech-in-noise hearing, but there is no evidence to suggest that genetic risk for hearing impairment affects cognition, according to results from a recently published study.
Results from the study also suggested that AD disease processes or a shared etiology may cause speech-in-noise difficulty prior to dementia onset.
Genetic risk score for AD (AD-GRS) was calculated as a weighted sum of 23 previously identified AD-related polymorphisms. Patients who had higher AD-GRS were significantly associated with poor speech-in-noise hearing (odds ratio [OR], 1.06; 95% CI, 1.01–1.11) and self-reported problems hearing with background noise (OR, 1.03; 95% CI, 1.00–1.05).
Lead author Willa Brenowitz, PhD, MPH, assistant professor, Center for Population Brain Health, University of California San Francisco, and colleagues found that poor speech-in-noise hearing (>-5.5 dB speech reception threshold; prevalence, 14%) was associated with lower cognitive scores (ß = –1.28; 95% CI, –1.54 to –1.03).
Investigators calculated a genetic risk score for hearing (hearing-GRS) using 3 previously identified polymorphisms related to hearing impairment. They found no significant association between hearing-GRS and cognitive scores (ß = –0.05; 95% CI, –0.17 to 0.07).
"Though we did not find evidence to support this the effect of hearing loss on cognition, our estimates were imprecise. Our findings suggest poor speech-in-noise hearing may be an early marker of underlying dementia processes,” Brenowitz et al. wrote. Effect sizes across all hearing outcomes ranged from a 2% to 13% increased odds of poor hearing per 1 unit increase in AD-GRS, essentially tripling the odds of AD while also increasing the risk of hearing impairment.
To evaluate whether AD-GRS predicted poor hearing and whether the hearing-GRS predicted worse cognition, Brenowitz and colleagues used age-, sex-, and genetic ancestry-adjusted logistic and linear regression models.
Data from UK Biobank participants without dementia aged 56 years and older with Caucasian genetic ancestry who completed a Digit Triplets Test of speech-in-noise hearing (n = 80,074), self-reported problem hearing and hearing with background noise (n = 244,915), and completed brief cognitive assessments were used in the analysis.
Higher AD-GRS with apolipoprotein E (APOE) was also associated with worse verbal reasoning, though, the AD-GRS without APOE was not. Additionally, the association of AD-GRS and poor speech in-noise hearing remained stable for patients with APOE (P <.02) and patients without (P <.02).
APOE alone was not significantly association with speech-in-noise reception threshold (SRT; OR, 1.04; 95% CI, 0.98–1.10). Notably, tests for horizontal pleiotropy of AD-GRS single-nucleotide polymorphisms (SNPs) with MR-Egger regression were not significant and intercepts were close to 0 for each outcome: self-reported problem hearing (ß = 0.000; standard error (SE), 0.000; P = .97), self-reported problem hearing in noise (ß = 0.004; SE, 0.002; P =.11), poor SRT (ß = 0.006; SE, 0.004; P = .18). SRT was on average –7.1 db (standard deviation [SD], 1.8), and 14% had poor speech-in-noise hearing (SRT > –5.5 dB).
Investigators of the study noted that additional research will be needed to replicate findings in other samples, to investigate measures of peripheral hearing loss, as well as to determine whether loss of speech-in-noise testing can be useful as a tool to identify preclinical AD.