Research in my laboratory is primarily focused upon the pathophysiology of glaucoma. The death of retinal ganglion cells in the glaucomatous retina elicits a neuroinflammatory reaction involving the release of TNF alpha and activation of the classical complement cascade. Neuroinflammation is a necessary process to remove cellular debris and reinstate tissue homeostasis, but there is also the danger that healthy cells can be damaged by the same process, leading to an acceleration of the disease.

One goal of my research is to determine if whether suppression of neuroinflammation in glaucoma is clinically beneficial or if the process should be left unimpeded. A second goal is to understand the events that lead to elevated intraocular pressure, a significant risk factor for the development of glaucoma. Intraocular pressure becomes elevated when the flow of aqueous humor through the trabecular meshwork becomes restricted. We are examining the role that the resident cells of the trabecular meshwork play in the process. We are also testing if replacing damaged or lost trabecular meshwork cells with stem cells that have been induced to mimic trabecular meshwork cells can regenerate this tissue and restore functional control of intraocular pressure in glaucomatous eyes.