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Brandon Cox, PhDBrandon Cox, PhD
Assistant Professor




Hearing loss is primarily caused by damage to specialized cells (called hair cells) that detect sound waves traveling through the cochlea of the inner ear.  Non-mammalian vertebrates, such as birds, fish, and amphibians, can regenerate their hair cells after damage, while damage to auditory hair cells in mammals is currently thought to be permanent. We have recently developed a genetic method to damage hair cells in the neonatal mouse in vivo and discovered that, in contrast to common belief, the mouse cochlea does have the capacity to regenerate its hair cells
after damage. However, when hair cell death was induced at one week of age, no evidence of regeneration was detected.

The goals of my laboratory are to build upon these findings and investigate the cell source, mechanism, and genes involved in hair cell regeneration in the neonatal mouse cochlea. We are also interested the developmental changes that take place during the first postnatal weeks that prevent regeneration from occurring in juvenile and adult mice. We use mouse genetics (Cre/LoxP and tetracycline inducible systems) to manipulate gene expression in specific cell types at specific ages, as well as fate mapping to trace the origin of the regenerated hair cells. 

YFP (green) labeled hair cells in the apical turn of the cochlea in Atoh1-CreER; Rosa26-YFP mice given tamoxifen at birth.

Newly regenerated hair cells in the neonatal mouse cochlea. Myosin VIIa (red) is a ubiquitous hair cell marker. Prestin (green) is specifically expressed in differentiated outer hair cells. EdU (white) labels cells that had previously divided.


Recent Publications