This is a hybrid event.

Noise-induced and age-related hearing loss in humans and animals: new insights and novel therapies

M. Charles Liberman, Ph.D., Schuknecht Professor of Otolaryngology, Harvard Medical School and Investigator, Eaton-Peabody Laboratories, Massachusetts Eye and Ear

Most types of hearing loss arise from damage to the sensory cells and/or neurons of the inner ear. In the normal ear, the sensory (hair) cells transduce sound-induced mechanical vibrations into electrical signals, and cochlear nerve fibers carry those signals to the brain. Hair cells degenerate during aging and after exposure to intense noise, and this impairs mechano-electric transduction such that stimulus intensity must be increased for sounds to be audible, as is routinely evaluated in a clinical audiogram.  It was long believed that hair cells were the most vulnerable elements in the ear and that cochlear nerve fibers die only after the hair cells have died.  We showed this was not true: the most vulnerable elements in both noise-induced and age-related hearing loss, in both human and animal ears, are the nerve terminals, specifically their synapses where the communication with hair cells takes place.  This synaptopathy can silence large numbers of cochlear nerve fibers, but it does not affect audibility, or the audiogram, until it is nearly complete. On the other hand, this nerve degeneration significantly impairs intelligibility, and likely explains why problems hearing in a noisy environment are so widespread.  From a therapeutic standpoint, it is exciting that synaptopathy leaves the hair cells intact, as well as the cell bodies and central projections of the cochlear neurons. Our animal work shows that raising intracochlear levels of a naturally occurring neurotrophin, by local delivery or gene therapy, can regenerate synapses after noise and reduce the age-related loss of synapses after middle age.  If successfully applied to humans, such therapies should greatly reduce the functional impairment of sensorineural hearing loss. 

Q&A and light refreshments following.

This lecture is made possible in part by a generous endowment from Professor Roger B. Loucks.