Research in my laboratory is aimed at understanding fundamental physiological properties of the eye and the pathophysiological mechanisms underlying a variety of complex eye diseases. Of primary interest are the glaucomas, a leading cause of blindness that affects approximately 70 million people worldwide. Glaucoma typically involves three types of events: molecular insults compromising the anterior chamber, increased intraocular pressure, and neurodegenerative retinal ganglion cell loss. Not surprisingly, the biological relationships linking these events are complex. Our approach for studying these events is founded in functional mouse genetics and supplemented by a variety of molecular, cellular, immunological, and neurobiological techniques. The premise for this approach is that stringently performed genetic studies offer great potential for overcoming the natural biological complexity of glaucoma.
Current projects in the lab involve mouse models of pigmentary glaucoma and are testing the hypotheses that aberrant melanosomal processes and inflammation are potent contributors to this form of glaucoma. We are also interested in new mouse models of glaucoma and are developing mouse ES cell based genetic strategies for fostering the discovery of new glaucomatous mechanisms. In the long term, these studies will contribute to an increased understanding of eye diseases such as glaucoma, and ultimately to improved human therapies.