Genetically Reducing AMPK Activity May Prevent Hereditary Hearing Loss

New Genetic Modification May Prevent Hearing Loss

Yale University research demonstrates that genetically lowering AMPK activity delays inherited hearing loss in mice.

New research from Yale University reveals that genetically reducing AMPK activity delays hereditary hearing loss in mice.

Hereditary hearing loss can worsen over time and lead to premature deafness. In a new study, a Yale-led research team successfully applied genetic modification to delay inherited hearing loss in mice.

Led by professor of pathology and genetics Gerald S. Shadel, the collaborative research team genetically altered mice to develop a model of hearing loss caused by a defect in mitochondria (specialized compartments within cells). Hearing loss in these mice was found to involve dysfunction in specialized tissues in the inner ear. The research team determined that activation of a stress-response enzyme called AMPK triggered this dysfunction. Genetically reducing AMPK activity (by knocking out one of its genes) had no impact on mice with normal hearing, but delayed or prevented hereditary hearing loss in the deafness-model mice.

While more research is needed, the study results point to possible strategies for preventing or treating deafness associated with mitochondrial dysfunction and aging in people. “This opens the possibility for intervention in humans based on inhibiting AMPK, which is already a drug target for several diseases,” stated Dr. Shadel.

The study was published online by The American Journal of Pathology. Other Yale authors include Sharen E. McKay, Wayne Yan, Jessica Nouws, Maximilian J. Thormann, Abdul Khan, Joseph Santos-Sacchi, and Lei Song. Co-author Nuno Raimundo is from the University Medical Center Goettingen in Germany.

Reference: “Auditory Pathology in a Transgenic mtTFB1 Mouse Model of Mitochondrial Deafness” by Sharen E. McKay, Wayne Yan, Jessica Nouws, Maximilian J. Thormann, Nuno Raimundo, Abdul Khan, Joseph Santos-Sacchi, Lei Song and Gerald S. Shadel, 6 November 2015, American Journal of Pathology.
DOI: 10.1016/j.ajpath.2015.08.014

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