Reported Hearing Loss in Alzheimer’s Disease Is Associated With Loss of Brainstem and Cerebellar Volume

Multiple epidemiological studies have revealed an association between presbycusis and Alzheimer’s Disease (AD). Unfortunately, the neurobiological underpinnings of this relationship are not clear. It is possible that the two disorders share a common, as yet unidentified, risk factor, or that hearing...

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Bibliographic Details
Published in:Frontiers in human neuroscience 2021-09, Vol.15, p.739754-739754
Main Authors: Llano, Daniel A., Kwok, Susanna S., Devanarayan, Viswanath
Format: Article
Language:English
Subjects:
Aging
Alzheimer's disease
Alzheimer’s
Atrophy
auditory
Brain research
Brain stem
brainstem
Cerebellum
Cognitive ability
College campuses
Dementia
Epidemiology
Ethics
Health sciences
Hearing loss
Hospitals
Human subjects
Magnetic resonance imaging
Medicine
Memory
Neurodegenerative diseases
Neuroscience
Oxidative stress
presbycusis
Review boards
Risk factors
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Summary:Multiple epidemiological studies have revealed an association between presbycusis and Alzheimer’s Disease (AD). Unfortunately, the neurobiological underpinnings of this relationship are not clear. It is possible that the two disorders share a common, as yet unidentified, risk factor, or that hearing loss may independently accelerate AD pathology. Here, we examined the relationship between reported hearing loss and brain volumes in normal, mild cognitive impairment (MCI) and AD subjects using a publicly available database. We found that among subjects with AD, individuals that reported hearing loss had smaller brainstem and cerebellar volumes in both hemispheres than individuals without hearing loss. In addition, we found that these brain volumes diminish in size more rapidly among normal subjects with reported hearing loss and that there was a significant interaction between cognitive diagnosis and the relationship between reported hearing loss and these brain volumes. These data suggest that hearing loss is linked to brainstem and cerebellar pathology, but only in the context of the pathological state of AD. We hypothesize that the presence of AD-related pathology in both the brainstem and cerebellum creates vulnerabilities in these brain regions to auditory deafferentation-related atrophy. These data have implications for our understanding of the potential neural substrates for interactions between hearing loss and AD.
ISSN:1662-5161
1662-5161
DOI:10.3389/fnhum.2021.739754