Willa D Brenowitz1, Teresa J Filshtein2, Kristine Yaffe2, Stefan Walter2, Sarah F Ackley2, Thomas J Hoffmann2, Eric Jorgenson2, Rachel A Whitmer2, M Maria Glymour2. 1. From the Department of Psychiatry and Behavioral Sciences (W.D.B., K.Y.), Department of Epidemiology and Biostatistics (K.Y., S.F.A., T.J.H., M.M.G.), Department of Neurology (K.Y.), and Institute for Human Genetics (T.J.H.), University of California, San Francisco; 23andMe (T.J.F.), Mountain View; San Francisco VA Health Care System (K.Y.), CA; Department of Medicine and Public Health (S.W.), Rey Juan Carlos University, Madrid, Spain; Kaiser Permanente Northern California Division of Research (E.J.), Oakland; and Public Health Sciences (R.A.W.), Division of Epidemiology, Alzheimer's Disease Research Center, UC Davis School of Medicine, CA. willa.brenowitz@ucsf.edu. 2. From the Department of Psychiatry and Behavioral Sciences (W.D.B., K.Y.), Department of Epidemiology and Biostatistics (K.Y., S.F.A., T.J.H., M.M.G.), Department of Neurology (K.Y.), and Institute for Human Genetics (T.J.H.), University of California, San Francisco; 23andMe (T.J.F.), Mountain View; San Francisco VA Health Care System (K.Y.), CA; Department of Medicine and Public Health (S.W.), Rey Juan Carlos University, Madrid, Spain; Kaiser Permanente Northern California Division of Research (E.J.), Oakland; and Public Health Sciences (R.A.W.), Division of Epidemiology, Alzheimer's Disease Research Center, UC Davis School of Medicine, CA.
Abstract
OBJECTIVE: To test the hypothesis that incipient Alzheimer disease (AD) may adversely affect hearing and that hearing loss may adversely affect cognition, we evaluated whether genetic variants that increase AD risk also increase problem hearing and genetic variants that increase hearing impairment risk do not influence cognition. METHODS: UK Biobank participants without dementia ≥56 years of age with Caucasian genetic ancestry 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. A genetic risk score for AD (AD-GRS) was calculated as a weighted sum of 23 previously identified AD-related polymorphisms. A genetic risk score for hearing (hearing-GRS) was calculated using 3 previously identified polymorphisms related to hearing impairment. Using age-, sex-, and genetic ancestry-adjusted logistic and linear regression models, we evaluated whether the AD-GRS predicted poor hearing and whether the hearing-GRS predicted worse cognition. RESULTS: Poor speech-in-noise hearing (>-5.5-dB speech reception threshold; prevalence 14%) was associated with lower cognitive scores (ß = -1.28; 95% confidence interval [CI] -1.54 to -1.03). Higher AD-GRS was 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). Hearing-GRS was not significantly associated with cognitive scores (ß = -0.05; 95% CI -0.17 to 0.07). CONCLUSIONS: Genetic risk for AD also influences speech-in-noise hearing. We failed to find evidence that genetic risk for hearing impairment affects cognition. AD disease processes or a that shared etiology may cause speech-in-noise difficulty before dementia onset.
OBJECTIVE: To test the hypothesis that incipient Alzheimer disease (AD) may adversely affect hearing and that hearing loss may adversely affect cognition, we evaluated whether genetic variants that increase AD risk also increase problem hearing and genetic variants that increase hearing impairment risk do not influence cognition. METHODS: UK Biobank participants without dementia ≥56 years of age with Caucasian genetic ancestry 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. A genetic risk score for AD (AD-GRS) was calculated as a weighted sum of 23 previously identified AD-related polymorphisms. A genetic risk score for hearing (hearing-GRS) was calculated using 3 previously identified polymorphisms related to hearing impairment. Using age-, sex-, and genetic ancestry-adjusted logistic and linear regression models, we evaluated whether the AD-GRS predicted poor hearing and whether the hearing-GRS predicted worse cognition. RESULTS: Poor speech-in-noise hearing (>-5.5-dB speech reception threshold; prevalence 14%) was associated with lower cognitive scores (ß = -1.28; 95% confidence interval [CI] -1.54 to -1.03). Higher AD-GRS was 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). Hearing-GRS was not significantly associated with cognitive scores (ß = -0.05; 95% CI -0.17 to 0.07). CONCLUSIONS: Genetic risk for AD also influences speech-in-noise hearing. We failed to find evidence that genetic risk for hearing impairment affects cognition. AD disease processes or a that shared etiology may cause speech-in-noise difficulty before dementia onset.
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