Visual and auditory sensory impairments differentially relate with Alzheimer’s pathology
Gihwan Byeon 1, Min Soo Byun 2, 3, Dahyun Yi 4, Joon Hyung Jung 5, Nayeong Kong 2, Yoonyoung Chang 2, MUSUNG KEUM 2, Gijung Jung 4, Hyejin Ahn 4, Jun-Young Lee 6, Yu Kyeong Kim 7, Koung Mi Kang 8, Chul-Ho Sohn 8, Dong Young Lee 2, 3, 4*
1Department of Neuropsychiatry, Kangwon National University Hospital, Chuncheon, Republic of Korea, 2Department of Psychiatry, Seoul National University College of Medicine, Seoul, Republic of Korea, 3Department of Neuropsychiatry, Seoul National University Hospital, Seoul, Republic of Korea, 4Institute of Human Behavioral Medicine, Medical Research Center, Seoul National University, Seoul, Republic of Korea , 5Chungbuk National University Hospital, Republic of Korea, 6Department of Neuropsychiatry, SMG-SNU Boramae Medical Center, Seoul, Republic of Korea, 7Department of Nuclear Medicine, SMG-SNU Boramae Medical Center, Seoul, Republic of Korea, 8Department of Radiology, Seoul National University Hospital, Seoul, Republic of Korea
Received: January 22, 2024; Revised: June 7, 2024; Accepted: June 25, 2024; Published online: June 25, 2024.
© The Korean College of Neuropsychopharmacology. All rights reserved.

Objective: We intended to investigate the relationships between visual sensory impairment (VSI) or auditory sensory impairment (ASI) and brain pathological changes associated with cognitive decline in older adults.
Methods: We primarily tried to examine whether each sensory impairment is related to Alzheimer’s disease (AD) pathology, specifically beta-amyloid (Aβ) deposition, through both cross-sectional and longitudinal approaches in cognitively unimpaired older adults. Self-report questionnaires on vision and hearing status were administered at the baseline. Neuroimaging scans including brain [11C] Pittsburgh Compound B PET and MRI, as well as clinical assessments, were performed at baseline and 2-year follow-up.
Results: Cross-sectional analyses showed that the VSI-positive group had significantly higher Aβ deposition than the VSI-negative group, whereas there was no significant association between ASI positivity and Aβ deposition. Longitudinal analyses revealed that VSI positivity at baseline was significantly associated with increased Aβ deposition over 2 years (β=0.153, p=0.025), although ASI positivity was not (β=0.045, p=0.518). VSI positivity at baseline was also significantly associated with greater atrophic changes in AD-related brain regions over the 2-year follow-up period (β=-0.207, p=0.005), whereas ASI positivity was not (β=0.024, p=0.753). Neither VSI nor ASI positivity was related to cerebrovascular injury, as measured based on the white matter hyperintensity volume.
Conclusion: The findings suggest that VSI is probably related to AD-specific pathological changes, which possibly mediate the reported relationship between VSI and cognitive decline. In contrast, ASI appears not associated with AD pathologies but may contribute to cognitive decline via other mechanisms.
Keywords: Dementia, Sensory impairment, Alzheimer, Amyloid