Common Contributing Causes to Age-Related Hearing Loss and Alzheimer's Disease

Age-related diseases arise from common causes, but aging is a multifaceted process of numerous interacting forms of damage and disarray, and it is usually challenging to assign a weight to any given part of aging in the causation of any given age-related disease. Still, a great deal of theorizing takes place. Here, researchers discuss the causes of hearing loss and Alzheimer's disease, given that the two conditions tend to co-occur more often than mere chance would lead to. Some underlying process contributes meaningfully to both, and in the treatment of aging, it is best to aim as close to the root causes as possible. That is where the greatest benefit will be achieved.

Epidemiological studies show a strong independent association between age-related hearing loss (ARHL) and Alzheimer's disease (AD). Actually, recent data link 9% of sporadic AD to hearing loss starting at mid-life. Thus, ARHL emerges as the main preventable risk factor of AD, at least in this life period, even with causal implications. Comorbidity between ARHL and AD will further aggravate the condition of the patients, multiplying health, social, economic, and sanitary impact. In sum, epidemiological data link ARHL with cognitive impairment and dementias, in particular AD, pointing to dynamic association between these two neurodegenerative conditions. Besides ARHL contributing to the pathogenesis of AD, the converse may also be the case. However, at present, the biological or mechanistic foundations of such interplay are unknown.

Several hypotheses/mechanisms have been put forth. These include existence of shared underlying pathologies, such as those of vascular origin; diminished auditory input that directly triggers brain atrophy as an expression of the complex chain of cellular events leading to dementia; overload of cognitive resources, diverted to process diminished auditory input; existence of amyloid plaques (AP), intraneuronal neurofibrillary tangles (NFT) and cytoskeletal pathology in the cochlea, dorsal cochlear nucleus, superior olive, central nucleus of the inferior colliculus, medial geniculate body, primary auditory cortex and association area of the auditory cortex. These or another related hypothesis/mechanism do not exclude each other mutually. Whether such interplay is unidirectional from ARHL to AD, or bidirectional is also unknown. The challenge of testing such intricate and open-end hypotheses scenery, is the complexity and multiplicity of factors involved in the genesis and development of both neurodegenerative conditions.

Frailty and related oxidative stress have recently drawn considerable attention. In this review, we discuss the possibility that the oxidative stress linked to frailty, could be, at least in part, primarily involved in the interplay between ARHL and AD.


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