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Associations and Potential Multiple Mechanisms between Subjective Hearing Loss and Cognitive Impairment
1Qi-Hao Guo, Department of Gerontology, Shanghai Sixth People's Hospital, Shanghai Jiao Tong University School of Medicine, 600 Yishan Road, Shanghai, 200233, China, Phone: +86 13817741448, E-mail: qhguo@sjtu.edu.cn; Fang Xie, Department of Nuclear Medicine and PET Center, Huashan Hospital, Fudan University, 518 East Wuzhong Road, Shanghai, 200040, China, Phone: +86 13818672745,
Background:
Subjective hearing loss (SHL) refers to an individual's self-assessment of their hearing loss. The association and underlying mechanisms between SHL and cognitive impairment still necessitate elucidation.
Objectives:
To validate potential mechanisms between SHL and cognitive impairment.
Design:
Cross-section.
Setting:
Shanghai, China.
Participants:
A total of 2369 individuals from communities and the cognitive disorder clinic.
Measurements:
All participants were subjected to a comprehensive neuropsychological assessment, encompassing the Hearing Handicap Inventory for the Elderly-Screening Version (HHIE-S). The participants' brain β-amyloid (Aβ) deposition status, plasma biomarkers associated with Alzheimer's disease (AD), and cardiovascular risk factors were also collected.
Results:
In individuals with a heightened SHL, elevated HHIE-S score was linked to diminished cognitive and daily functioning as well as heightened levels of depressed mood. This correlation was observed in auditory memory performance but not in visual memory. The influence of SHL on cognitive function was mediated by depressed mood. SHL was associated with diabetes and smoking, whereas cognitive function was associated with hyperlipidemia and alcohol consumption. In individuals with positive brain Aβ deposition, SHL demonstrated associations with cognitive function independent of plasma Aβ42/40 ratio, P-tau181, neurofilament light chain, and APOE allele status.
Conclusion:
SHL has an independent effect on cognitive impairment. The findings do no provide evidence for the common cause mechanism. Instead, the findings support the presence of a cognitive resource mechanism and an impoverished environment mechanism, along with the potential for a pathological interaction mechanism.
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