“This is really a very frustrating clinical problem when you sometimes don’t have very much to offer the parents,” she added.
Andrew J. Griffith, MD, PhD, chief of the molecular biology and genetics section of the otolaryngology branch of the National Institute on Deafness and Other Communication Disorders in Bethesda, Md., part of the National Institutes of Health, discussed how his laboratory has developed a mouse model with SLC26A4 gene mutations that mimic the human phenotype of hearing loss fluctuation. The mutations can cause hearing loss related to enlarged vestibular aqueducts.
SLC26A4 knockout mice are totally deaf and are not a good model for studying the typical human phenotype. But Dr. Griffith’s lab has developed a model in which the expression of SLC26A4 is controlled by putting the antibiotic doxycycline in the mice’s drinking water during the formation of the embryo (Neurobiol Dis. 2014;66:53-65).| ← Previous | | | Next → | Single Page