Researchers at the University of Michigan’s Kresge Hearing Research Institute and U-M’s C.S. Mott Children’s Hospital discovered that mutations in connexin 26 gene are a leading cause of genetic hearing loss. They also discovered that enhanced diet had the opposite effect on another mutant mouse modeling AUNA1, a rare type of hearing loss.

“Many babies born with a genetic mutation that causes deafness pass their newborn screening test but then lose their hearing later in life,” says author Glenn Green, M.D., associate professor of pediatric otolaryngology at C.S. Mott Children’s Hospital.

These patterns suggests potential opportunity to save cells present at birth for some children. “Our findings suggest that a particular high dose of mineral and vitamin supplements may be beneficial to one genetic mutation,” adds senior author Yehoash Raphael, Ph.D., professor in the Department of Otolaryngology-Head and Neck Surgery at the University of Michigan Medical School.

“However, the negative outcome in the AUNA1 mouse model suggests that different mutations may respond to the special diet in different ways.”

The study was conducted on mice. They received antioxidant regimen post-natally and in utero in separate experiments. For the mice with the connexin 26 mutations, enhanced diet was associated with a slower progression of hearing loss. However, mice with the AUNA1 gene mutation experienced accelerated progression of deafness post diet.

Antioxidant treatment has also been shown to preserve gap junctions, which are the cellular components directly impacted by loss of connexin 26.

“These findings are encouraging for those of us who treat children with progressive connexin 26 hearing loss, and possibly for other mutations not yet tested. Further studies are needed to confirm these findings in children and to explore whether oral administration of antioxidants could someday be considered as an effective treatment.” says Green.

Source: Coherent News
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