There is a correlation between hearing loss and progression of dementia via conditions such as Alzheimer's disease. It remains an open question as to the direction of causation in this relationship - or indeed whether there is little to no causation, and this is a case of two independent manifestations of the same underlying process of damage and dysfunction. Many aspects of aging are correlated simply because aging is, at root, caused by the accumulation of a small number of forms of cell and tissue damage. If a greater degree of any one type of damage is present, then all of the consequences of that damage will tend to be further advanced and more severe.
Age-related hearing loss (ARHL) has been considered as a promising modifiable risk factor for cognitive impairment and dementia. Nonetheless, the relationship between ARHL and Alzheimer's disease (AD) is still controversial. Besides the insufficient statistical power due to small sample size, their relationship might be further complicated by misclassification bias due to misdiagnosis, given that (1) AD was defined in previous observational studies mostly without pathological evidence, such as amyloid PET imaging or cerebrospinal fluid (CSF) biomarkers; (2) aged subjects with hearing loss (HL) might be more intellectually capable than the cognitive tests suggest. Therefore, investigating the association between ARHL and AD biomarkers might be less biased and more informative about the causal relationship.
Degeneration of the auditory system was reported in AD decades ago. In addition to confirming the prior findings that ARHL is associated with temporal lobe atrophy, we demonstrated for the first time, a strong link between ARHL and the amount of tau and phosphorylated tau (ptau) in CSF as well as reserve capability of entorhinal cortex. These influences seemed to be more obvious in the non-demented stage of the AD continuum. We did not find a significant relationship between ARHL and Aβ levels.
While AHRL can contribute to depression that may exacerbate the cognitive impairment and neurodegeneration biomarker profile, our results suggested that the neurodegenerative effects of ARHL might be driven by accelerating cerebrospinal fluid tau levels and atrophy of entorhinal cortex. Furthermore, our findings suggest that prevention or management of ARHL in preclinical and prodromal stage of AD might be effective in combating neurodegeneration.