A team of researchers found that using DNA as a drug – commonly called gene therapy – in laboratory mice may protect the inner ear nerve cells of humans suffering from certain types of progressive hearing loss.
A wide spectrum of people are affected by hearing loss and the way each person deals with it is highly variable.
“We tried to figure out why the mouse was losing cells that enable it to hear. Why did it lose its hearing? The collaborative work allowed us to provide gene therapy to reverse the loss of nerve cells in the ears of these deaf mice,” said professor Karen B. Avraham from Tel Aviv University’s Sackler Faculty of Medicine.
Along with Yehoash Raphael from University of Michigan, Avraham and doctoral student Shaked Shivatzki created a mouse population possessing the gene that produces the most prevalent form of hearing loss in humans – the mutated connexin 26 gene.
Mice with the mutated connexin 26 gene exhibit deterioration of the nerve cells that send a sound signal to the brain.
The researchers found that a protein growth factor used to protect and maintain neurons, otherwise known as brain-derived neurotrophic factor (BDNF), could be used to block this degeneration.
They then engineered a virus that could be tolerated by the body without causing disease, and inserted the growth factor into the virus.
Finally, they surgically injected the virus into the ears of the mice. This factor was able to ‘rescue’ the neurons in the inner ear by blocking their degeneration.
“It has important implications for the enhancement of sound perception with a cochlear implant used by many people whose connexin 26 mutation has led to impaired hearing,” Raphael added.
Inner ear nerve cells facilitate the optimal functioning of cochlear implants.
“Practically speaking, we are a long way off from treating hearing loss during embryogenesis. But we proved what we set out to do: that we can help preserve nerve cells in the inner ears of the mouse,” Avraham noted.
This already looks very promising, he said in a paper published in the journal Complex Human Disease.