Robert W. Nickells, PhD

Keywords: Glaucoma, BAX protein regulation

Education
PhD 1987, University of Calgary
BS 1983, Univeristy of Victoria
Postdoctoral Fellowship 1987-90, California Institute of Technology

Research Interests:
Glaucoma is one of the leading causes of blindness world-wide. Although an increase in intraocular pressure is often associated with this disease, it is marked by the progressive degeneration of retinal ganglion cell axons, which make up the optic nerve, and the apoptotic death of retinal ganglion cell bodies in the retina. Much of this work has centered around the critical function of the pro-apoptotic gene Bax, which is a critical mediator of mitochondrial dysfunction during this cell death process. Using Bax-depleted or deficient mice, the lab has demonstrated an absolute dependence of ganglion cell soma degeneration in both acute models of optic nerve injury, and in more chronic models of genetically induced ocular hypertension and glaucoma in these animals. Interestingly, in glaucoma, axonal degeneration is only retarded in mice that have somas completely resilient to degeneration. Dr. Nickells has now focused much of his research on better understanding the mechanisms of BAX protein activation in retinal ganglion cells, and whether or not the intrinsic apoptotic program occurs independently in ganglion cell axons. The ultimate goal is to develop a therapeutic that targets and inhibits BAX protein function in the hope of preventing neuronal loss in the retina in a way that may extend to many different neurodegenerative diseases.

Publications
PubMed Listing of Publications