Age Related Hearing Loss
Age-related hearing loss affects up to half of people over the age of 65. The onset of hearing loss for some can occur before the age of 65, which can affect the ability to work, leading to higher rates of unemployment. With our society’s aging demographics, age-related hearing loss is set to become an increasing problem that can cause social isolation, depression and perhaps even an acceleration of dementia. Furthermore, with so many people now listening to personal listening devices for extended periods at high volume, the problem is likely to increase, with earlier onset becoming more common. Consequently, the impact of hearing loss amongst those still in work is increasing and is beginning to be studied more widely.
The key complaint for those suffering from age-related hearing loss is difficulty understanding speech, in particular in noisy environments, or where several people are talking at the same time, such as at social gatherings. Understanding speech requires not only that the speech is heard, but also importantly that the different components of speech can be distinguished (for example, the difference between a “b” and “p” sound). These components can be very fast and rely on optimal function of auditory processing mechanisms in the brain as well as on reception by hair cells in the cochlea.
With aging, hair cells are lost and the signal reaching the brain reduces. Combined with this, a deterioration of central auditory processing and the decline of cognitive capacity can add to the problem. Evidence that age-related hearing loss is due as much to problems in the brain as to loss of hair cells in the cochlea comes from the finding that some people who have near perfect audiograms may still struggle to understand speech in environments where there is a lot of background noise.
There are no current treatment options. Hearing aids or cochlear implants can help some sufferers, although often interpreting speech remains a challenge.
A cochlear implant is a surgically implanted electronic device that provides a sense of sound to a person who has profound hearing loss. A cochlear implant does not cure deafness or hearing impairment, but is a prosthetic substitute which directly stimulates the auditory nerve. Cochlear implants bypass the normal hearing process; they have a microphone and some external electronics, generally behind the ear, which transmit a signal to an array of electrodes placed within the cochlea, which stimulates the auditory nerve. As of December 2012, approximately 324,000 people worldwide had cochlear implants surgically implanted, with roughly 58,000 adults and 38,000 children in the US. There are over 12,000 in the UK.
How Hearing Works
Sound is translated into neural signals by sensory hair cells in the cochlea. These hair cells turn the acoustic vibrations into electrical impulses that travel along the auditory nerve to the brain. The neural signals from each ear are then processed and integrated within the auditory brain stem to extract information about the direction of the sound source and its loudness. Centres in the mid-brain then filter the sound signals to focus on the important sounds; the selected signals are then received by the auditory cortex where they are interpreted, for example, to extract meaning from speech.
Treating disorders of central auditory function through Kv3 ion channel modulation
“Extracting the detailed features of sounds from auditory input via the cochlear requires neural circuits in the auditory brainstem that can encode sub-millisecond timing differences with high fidelity. Auditory brainstem and midbrain neurons meet these demands by expressing unique synaptic architecture, precisely tuned inhibitory circuits and a variety of biophysical specializations such as the expression of voltage-gated potassium (Kv) channels with rapid activation kinetics. Aging, ototoxic drugs, and environmental noise exposure can damage these specialised neural circuits, thereby reducing the bandwidth of information that can be transmitted from the ear to the brain. The neural circuits can compensate by decreasing local inhibition and increasing central gain. This compensatory plasticity restores higher auditory coding and perceptual awareness of basic acoustic features, but offers comparatively little benefit for the fine-grained temporal analysis, and may also lead to phenomena such as tinnitus.”
“The amount and type of Kv channels expressed in the cell membrane are major determinants of its intrinsic electrical excitability. Kv channels control the resting membrane potential as well as the shape, number, rate and timing of action potentials initiated in response to a stimulus. Kv3.1, a member of the Shaw class of Kv channels, is a high-threshold delayed rectifier channel that is widely expressed in fast spiking neurons throughout the auditory brainstem. Kv3.1 rapidly repolarizes the membrane potential during an action potential, effectively shortening the refractory period and thus enabling neurons to sustain high firing rates in response to high-frequency synaptic inputs. Kv3.1 current is regulated by auditory afferent input in auditory brainstem nuclei, and may be pathologically reduced following noise exposure or with age. Consequently, compounds that increase Kv3.1 currents by shifting the voltage-dependence of activation of the channels to more negative potentials, may be useful in the treatment of hearing disorders associated with central auditory pathology.”
(adapted from Chambers et al. 2017, Scientific Reports)