A Bidirectional Relationship Between Hearing Loss and Cognitive Decline?
In today's open access review paper, researchers lay out summarize hypotheses and evidence for there to be a bidirectional relationship between age-related hearing loss and loss of cognitive function. Their summary is informative, but in their view the present literature is too sparse to be conclusive, and further studies are needed to provide a greater breadth of human data.
There is good reason to think that hearing loss contributes directly to a more rapid pace of cognitive decline. The brain is very much a "use it or lose it" organ, and lacking use in later life, it declines more rapidly. Evidence from study populations with age-related hearing loss have compared the trajectories of those fitted with hearing aids versus those who were not, showing a greater incidence of dementia in those without augmented hearing.
When it comes to causation in the other direction, much of the thinking centers around common cause mechanisms of neurodegeneration. The same issues of chronic inflammation and cellular dysfunction that harm the brain also harm the sensory hair cells of the inner ear and their connections to the brain. It is also possible that complex issues situated entirely in the aging brain may contribute to difficulties in processing of auditory information that appear very similar to hearing loss.
Age-related hearing loss (ARHL), caused by peripheral hearing loss or central auditory processing disorder (CAPD), is the third leading cause of chronic disability in the older population. ARHL is one of the most important modifiable risk factors for dementia. Cumulative evidence links peripheral ARHL and cognitive decline with impaired performance across multiple cognitive domains, including episodic memory and processing speed. An independent association was also observed between subclinical hearing loss and cognitive impairment in a cross-sectional population study. A longitudinal cohort study further indicated that subjects with worse subclinical hearing loss have a steeper cognitive decline, as measured by the Digit Symbol Substitution Test over a mean follow-up of 9.1 years. However, a direct causal effect of peripheral hearing loss on dementia with hearing alterations is not defined. In a large cohort of cognitively healthy older people, peripheral hearing dysfunction was not associated with the pathological hallmark brain amyloid deposition of Alzheimer's disease (AD), the main phenotype of dementia. Age-related CAPD may precede the onset of clinical dementia in people with probable AD and might be an early marker of mild cognitive impairment (MCI) and AD. Older individuals with CAPD had a high risk for the subsequent onset of probable AD, and CAPD was independently associated with cognitive frailty, a frailty phenotype defined by coexisting physical frailty and MCI.
Accumulating evidence suggests that neurodegenerative pathologies add disproportionate central hearing deficits to any already existing peripheral hearing loss. Clinical findings have indicated that central auditory processing is impaired in people diagnosed with AD and its preclinical stages and may manifest many years before clinical diagnosis. Patients with semantic dementia frequently reported tinnitus and hyperacusis and were found to have abnormal neuroanatomical alterations in cortico-subcortical auditory network and limbic network. The prevalence of auditory hallucinations in Parkinson's disease and in dementia with Lewy bodies is estimated to be 8.9% and 30.8%, respectively. Neuropathological findings have indicated that AD pathological hallmarks, i.e., amyloid plaques and neurofibrillary tangles (NFTs), presented in the higher structures of the central auditory pathways and primary and secondary auditory cortical areas, but did not in the cochlea and cochlear nucleus. CAPD was persistently associated with cerebrospinal-fluid (CSF) tau levels, entorhinal and hippocampal cortex volumes, cortical thickness, and cognitive deficits in cognitively and physically healthy individuals with positive AD family history. These neuropathological alterations suggest that AD-related CAPD might not have resulted from peripheral hearing loss and induced maladaptive plastic changes.
Several hypotheses of possible etiological mechanisms have been proposed that elucidate these relationships. The common-cause hypothesis involves neurodegenerative, metabolic, and vascular pathophysiological alterations and chronic systemic inflammation during aging. The cognitive-reserve depletion or cascade hypothesis is based on brain experience-dependent neuroplasticity, cognitive reserve, and brain reserve, which refer to individual differences in the functionality and structure of the brain. The cognitive-load hypothesis proposes that individuals with hearing loss use greater cognitive resources for listening to degraded auditory signals and auditory perceptual processing, which makes these resources unavailable for other cognitive tasks, eventually leading to cognitive reserve depletion. Another hypothesis is proposed to further explain the neuropathological basis of cognitive load resulting in a vicious cycle of brain structure alterations, cognitive reserve and auditory reserve depletion. The hypothesis proposes a mechanism for the interaction between the medial temporal lobe related to auditory processing and dementia pathology, which could explain the association between hearing loss and cognitive impairment.