Association of Subjective Hearing Loss and Apolipoprotein E ε4 Allele on Alzheimer's Disease Neurodegeneration. Issue 1 (January 2021)

• Record Type: Journal Article
• Authors: Neff, Ryan M.; Jicha, Gregory; Hawk, Gregory S.; Bush, Matthew L.; McNulty, Beth
• Is Part Of: Otology & neurotology. Volume 42:Issue 1(2021)
• Publication Date: 2021-01
• Subjects: Age related hearing loss -- Alzheimer's disease -- Apolipoprotein -- Apolipoprotein E -- Apolipoprotein E4 -- Dementia -- Hearing loss; Otology -- Periodicals; Ear -- Diseases -- Periodicals; Skull base -- Surgery -- Periodicals; 617.8005
• DOI: 10.1097/MAO.0000000000002855
• Languages: English
• ISSNs: 1531-7129

Abstract

Abstract : Objective: Hearing loss (HL) and apolipoprotein E ε4 (ApoE4) allele are both dementia risk factors. No research has investigated the association of these variables regarding dementia, specifically Alzheimer's disease. Our goal was to evaluate HL and ApoE4 allele positivity toward degree of Alzheimer's neurodegeneration. Study Design: Retrospective. Setting: Academic. Patients: Alzheimer's neuropathology obtained from brain tissue databank. Documented demographics, subjective hearing status, cognition, and ApoE4. Subjects divided into four groups based on hearing status and ApoE4 positivity. Main Outcome Measures: Differences in cognition (clinical dementia rating, mini mental state examination (MMSE), geriatric depression score) and Alzheimer's neuropathology staging (Braak, CERAD) between groups. Results: Two-hundred and fifty-nine subjects. No significant difference between groups, with regard to hearing status or ApoE4 positivity, in premorbid cognition, including scores for clinical dementia rating and MMSE ( p = 0.2332). HL subjects had less severe neuropathology, as compared with normal hearing subjects. For example, high grade Braak stage was present in 27.1 and 51.0% of HL and normal hearing subjects, respectively ( p = 0.0263). This finding was in context of equivocal clinical cognition between groups. ApoE4+ individuals had more severe neurodegeneration; for example, 65.7 and 33.5% with high grade Braak stage for ApoE4+ and ApoE4– subjects, respectively ( p < 0.0001). Conclusion: Subjective HL subjects had less severe neuropathology with no difference in cognition, suggesting an additive effect of HL to cognitive burden of Alzheimer's neuropathology. HL appeared to increase cognitive burden, but wasn't manifested by greater neurodegeneration. This is clinically relevant in that treating HL could slow Alzheimer's disease progression.