Our current research interests concern both developing and aging brain function related to hearing and balance, neurodegeneration, and neuro-immune responses using murine transgenic models. More specifically, research in my laboratory is investigating how the regulation of calcium signaling contributes to hearing loss, development and maturation of sensory organs, and nerve regeneration.
Hearing loss affects a vast amount of people. Approximately 15% of Americans adults between the ages of 20 and 69 have high frequency hearing loss due to exposure to loud sounds and 50% of Americans over 75 years old are affected by presbycusis (https:// www.nidcd.nih.gov/health/statistics). Although substantial progress has been made in determining the genetic and cellular functions disrupted by acquired hearing loss, comparatively little is known about its underlying causes. It is known that both noise-induced hearing loss (NIHL) and age-related hearing loss (ARHL) involve outer hair cell (OHC) loss and dysfunction. The OHCs are one of the most prominent targets of noise and aging defects. Loss of OHCs leads to elevated hearing thresholds, along with loss of cochlear frequency tuning. Studies in our laboratory have focused on the development, maturation, and aging of the OHCs.
Our approach to helping solve this problem is through studying the function of a calcium binding protein, oncomodulin (Ocm), which is a member of the parvalbumin gene family. Its distribution is highly restricted, being mostly limited to a subset of sensory hair cells, specifically the OHCs, in the mammalian inner ear and elsewhere to a subset of immune cells (macrophages and neutrophils). Targeted deletion of Ocm in mice leads to hearing loss and to slowed or delayed nerve regeneration.
Our Team – January 2018
Left to right: Top row: Dr. Dwayne Simmons, Jemima McCluskey, Brianna Walker. Middle row: Preston Simpson, Taronish Madeka, Kelsey Chaykowski. Bottom Row: Craig Heflick, Andrew Cox, Matthew Tateossian.