Research suggests four reasons why adult-onset hearing loss is linked to dementia. Below we’ll take a brief look at the theories for why they are linked.
Shared Pathways
The ascending auditory pathway from the cochlea shares a pathway with the auditory cortex starting at the brainstem level. Even more importantly, both depend on optimal blood flow to function normally. When someone has compromised vascular function, the hair cells in the cochlear that transmit sound to the hearing nerve become damaged, resulting in hearing loss. That same vascular function contributes to normal cortical function, and when it is reduced or compromised, it is associated with vascular dementia. One abnormality can lead to two difficulties, one at the brain level and one at the ear level.
Reduced stimulation
The auditory pathway going up to the brain is dedicated to transmitting sound from the ear to the brain. What happens when sound is no longer being transmitted along the route, or it’s a much weaker signal? This leads to auditory deprivation, where the brain structure dedicated to a hearing becomes weakened from a lack of neural activity and stimulation over time. Researchers found that the change in brain function from auditory deprivation can be a risk factor for dementia.
What’s so bad about auditory deprivation anyway?
Not only is auditory deprivation a result of lack of stimulation from peripheral hearing, but it also contributes to the brain having less access to verbal and emotional input from speech, which provides critical cues for interpreting complex social interactions. This reduction in being able to interpret complex listening environments can negatively affect brain function and brain structure. Auditory deprivation can also cause people to pull back
from engaging in difficult social situations. Reduced social interaction is a risk factor for dementia in later years, as is general inactivity.
Increased cognition needed for hearing
People with hearing loss use more cognitive resources for listening. This, in turn, means that our brain resources are unavailable for other uses, such as for interpreting higher-level interactions. It also means we no longer have the same resources, like attention, working memory, and language processing. This may cause changes in brain activity related to difficult listening cause that can lead to irreversible degenerative damage.
There is a fixed capacity for many cognitive functions. When we use up our resources for listening in harder-to-understand environments, it means we have fewer resources available for other functions, like working memory. Think about it; if you can’t hear something, then you’re far less likely to remember it. Or if you hear something so softly that your brain doesn’t interpret it as important and immediately files it away as not important.
Auditory deprivation is less stimulation, and the third reason indicates more stimulation. How does this tie into dementia?
Auditory deprivation causes changes in the neural pathways and changes in the actual brain structure years before dementia is even on the radar. But these changes in neural pathways can cause an increased risk of subsequent dementia. The increased resources being used for listening may then lead to cognitive deficits. Both have different neural outcomes, but both are tied to the possible onset of dementia.
What effect does hearing intervention have on dementia onset? It’s unclear to researchers whether dementia is reversible. At this point, there is no proof of a way to reverse the onset. However, there are things people can do as preventative measures to delay the damage to cognitive functioning. One of those things is to wear hearing aids if you have hearing loss.
Proactive changes, like wearing hearing aids for your hearing loss, mean that you are giving yourself the best opportunity to keep your auditory brain active and robust.
Don’t you want to give yourself the best chance to live your best life?
If so, then give us a call today.
Resource credit:
Griffiths, Timothy D et al. “How Can Hearing Loss Cause Dementia?.” Neuron vol. 108,3 (2020): 401-412. doi:10.1016/j.neuron.2020.08.003
