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Genetic hearing loss may be reversible without gene therapy

the two connexins just cut the supply for making the gap junctions in half."

By adding extra connexin26 to mice that were missing connexin30, Dr. Lin and his team proved the latter hypothesis. With the additional connexin26, hearing sensitivity was restored and the expected hair cell death never occurred. Those positive findings led Dr. Lin to conclude, "The problem is simply caused by not having enough protein remaining in the ear of these mutant mice to assemble gap junctions."

Dr. Lin and his colleagues are now working to see if connexin-related deafness can be reversed in a mouse model, or if increasing connexin30 may help when connexin26 is absent.

As the research picks up momentum, these results--and future findings--may mean big changes for how congenital deafness is approached. Up to now, says Dr. Lin, scientists working on hearing loss had placed all their bets on gene therapy. That may no longer make sense. "Gene therapy, which has very few successful cases so far, may not be necessary," explains Dr. Lin.

Instead, Dr. Lin's findings indicate that a drug to boost connexin26 may be all that is needed. "Our work predicts that a drug should be sufficient to cure connexin30 deletion-caused deafness," he says.


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Contact: Holly Korschun
hkorsch@emory.edu
404-727-3990
Emory University
22-Feb-2007


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