By Ruili Xie, Ph.D.
Age-related hearing loss (ARHL), also known as presbycusis, is one of the most prevalent health conditions affecting older adults. The leading cause of ARHL is generally attributed to damage in the ear during aging, which include the loss of the inner ear’s sensory hair cells and spiral ganglion cells (SGCs).
Hair cells act like antennae for the auditory system to receive sound information from the environment. SGCs are the nerve cells that connect the ear and the brain, with their peripheral branches receiving sound information from hair cells, and their central branches forming the auditory nerve to pass information to the brain. Recent studies showed that the terminals (endpoints) of SGC peripheral branches are vulnerable and can be damaged during aging, which are thought to be the primary cause of ARHL.
However, the majority (over 70 percent) of SGC peripheral terminals survive normal aging. It is unclear whether, with age, sound information is reliably transmitted through the surviving SGCs to the brain; and if not, how this may contribute to ARHL.
One particular point of interest lies in the terminals of the SGC central branches (the auditory nerve synapses) that activate their target neurons in the brain. Deterioration in the information flow at these synapses with age would reduce sensory input to the brain and lead to ARHL.
For the first time, Dr. Paul B. Manis and I have found that the transmission of information from SGCs to their target neurons in the cochlear nucleus (the first auditory station in the brain) is compromised in aged mice with ARHL. The transmission process deteriorates due to abnormal calcium signaling at the central terminals of the SGCs. The study not only proposes a novel brain mechanism that underlies ARHL, but also provides new strategies in developing future clinical treatments.