Evidence that the workings of the inner ear can be regenerated to treat a common cause of deafness is published today.
An American team reports a way to trigger the growth of new hair cells in the inner ear – the sensory cells that pick up sound vibrations that are lost as a result of ageing, disease, certain drugs, and the cacophony of modern life.
The new understanding, which one day could help millions of people worldwide, is published today in the journal Nature by Dr Neil Segil and colleagues at the House Ear Institute in Los Angeles and University of Southern California, Los Angeles.
They have shown that "supporting cells" from the postnatal mouse inner ear retain the ability to divide and turn into new sensory hair cells in culture.
Named after the hair-like projections on their surfaces, hair cells form a ribbon of vibration sensors along the length of the cochlea, the spiral, seashell like structure in the inner ear that detects sound. Receiving vibrations through the eardrum and bones of the middle ear, hair cells convert them to electrical signals carried to the brain.
Unlike birds and other lower vertebrates, which can regenerate hair cells, however, humans and other mammals get one set, and that is it.
Normally, humans are born with about 12,000 hair cells in each ear and the death of the cells accounts for most types of acquired hearing loss. Overall, the steady loss that accompanies the wear and tear of ageing produces significant hearing deterioration in about a third of the population by the age of 70.
The research strongly suggests that the cochlea of mice and men retains the capacity for regeneration, but that the signals for regeneration are either absent or actively inhibited in the body.
When birds regenerate their hair cells, a supporting cell divides to make two daughters, one of which turns into a hair cell. The team found supporting cells from mice that are able to divide have turned off a protein called p27. By developing drugs to inhibit p27, it may be possible to stimulate hair cell growth.
"Our discoveries provide one important target for potential therapeutic intervention in the future," said Prof Segil.
Source: Telegraph Newspaper Online, June 22, 2006