About

Glaucoma-related vision loss

Our aim is to prevent, reverse, or stop the progression of vision loss that occurs during glaucoma. We study the physiology, pharmacology, biochemistry, morphology, neural control and aging of the fluid formation and drainage pathways in the eye. We seek to understand how and why people develop glaucoma (a pressure-dependent degeneration of the optic nerve that carries visual images from the eye to the brain, and is the most common cause of irreversible visual loss globally) and identify potential new therapeutic interventions. We study the mechanism of action of different classes of glaucoma therapeutics and their additive properties. Most patients will use more than one class of drug over their lifetime, and typically use several classes concurrently. We seek to develop viral vector / gene transfer strategies that would offer long-term reduction of intraocular pressure (IOP), the leading causal risk factor for glaucoma, while eliminating the burden of multiple daily self-administered eye drops. Our goal is to deliver a drug, protein or gene into the cells of the aqueous humor outflow pathways of the eye. The products of these genes, working inside specific eye cells, will potentially enhance aqueous humor outflow and lower intraocular pressure, a major causal risk factor for the development and progression of glaucoma-related vision loss. Having the patient as part of the delivery system engenders poor compliance and sub-optimal outcomes; we think gene therapy can do better.

Kaufman Lab Members