Genes on Chromosome 17 of Mice Contribute to Age-Related Hearing Loss

Presbycusis, the loss of hearing associated with aging, is one of the main causes of acquired deafness, which affects more than 37 million Americans.  With the increased life expectancy of the human population, hearing loss is likely to be more prevalent and a widespread public health concern.  Genetic studies in both humans and mice have shown that specific genes can contribute to presbycusis.  Our laboratory discovered that inbred mouse, 129S6/SvEvTac (S6), has early-onset, age-related hearing loss, providing a model of presbycusis.   Our goal is to use this mouse to improve our understanding of the physiological and genetic mechanisms associated with age-related hearing loss. Preliminary results allowed us to hypothesize that gene(s) that contribute to hearing loss in this strain are present on chromosome 17.  To address these questions, we measured the hearing sensitivity of S6 mice over a range of frequencies using auditory brainstem responses (ABRs).  We also used selective breeding and traditional genetic approaches to determine the location and genetic characteristics of the causal gene(s).   Our results support the hypothesis that hearing loss genes are present on Chromosome 17, specifically within the proximal 30-megabase region of the chromosome.  Furthermore, these gene(s) contribute selectively to high-frequency hearing loss in the S6 strain.   These findings in mice will provide a better understanding of the genes and the mechanisms involved with age-related hearing loss thereby elucidating homologous genes in humans that may contribute to presbycusis.