Uncovering Disease Pathophysiology to Improve Treatments
Featured News // News // Patient Care // Research News // Tele-Ophthalmology // Jan 18 2017
Paul Kaufman, MD and researcher B’Ann Gabelt, MS
Meet Paul Kaufman, MD, Glaucoma sub-specialist at the University of Wisconsin Department of Ophthalmology and Visual Sciences
January is National Glaucoma Awareness Month
Meet Paul Kaufman, MD, glaucoma clinician-researcher at the University of Wisconsin Department of Ophthalmology and Visual Sciences
Dr. Kaufman has multiple research interests centered on the aging eye. His lab is investigating mechanisms of primate aqueous humor formation and drainage systems and how they may be manipulated to reduce intraocular pressures in glaucoma. Dr. Kaufman also researches the dynamics of the accommodative apparatus in the eye that is lost in aging patients (presbyopia, the age-related inability to focus on very near objects). His research seeks to gain understanding of the pathophysiology of glaucoma and presbyopia to develop novel pharmacologic therapies for the human form of both diseases.
Glaucoma, the second leading cause of vision loss in Americans, is a characteristic degeneration of the optic nerve, which transmits visual impulses from the eye to the brain. Elevated fluid pressure within the eye is the most important causal risk factor, damaging the nerve in a variety of ways leading to eventual blindness. This disease can go undiagnosed, as it is asymptomatic in the early stages. Many people may have the disease and not know it until permanent damage has occurred.
The resistance to fluid drainage out of the eye increases with age and in glaucoma. Variations or excesses in normal aging processes may shift the balance toward the initiation of glaucoma and its progression. These processes can result in accumulation of extracellular material, and in stiffening, in the outflow pathways, which contributes to the increased resistance to outflow and the resultant increase in intraocular pressure. We know that each time the ciliary muscle contracts, as the eye attempts to accommodate for near focus, it spreads the meshwork and widens the canal, thus allowing fluid to pass through the meshwork and exit the eye more easily. The loss of ciliary muscle mobility with age may cause this drainage network to clog, resulting in increased pressure in the eye and glaucoma. Our laboratory is actively involved in developing novel therapeutic strategies for glaucoma in both the pharmacologic and gene therapy arenas.
Presbyopia, the age-related loss of accommodation, or the ability to focus on near objects, is the most common ocular affliction in the world, affecting every individual over the age of 45-50 years. We believe that its pathophysiology may be linked to that of glaucoma. Accommodation, the process by which the eye focuses on near objects, occurs in humans through the controlled alteration of the crystalline lens. The classic theory for the development of presbyopia involves a progressive hardening of the lens with aging. However, recent and ongoing research points to another contributor. As the eye changes focus, the ciliary muscle contracts, allowing the lens to thicken. The ciliary muscle attaches to the back of the eye via an elastic network. This membrane becomes less elastic with age, rendering ciliary muscle contraction less effective in promoting lens thickening. As the ciliary muscle ages, its ability to move is progressively restricted, so that when it contracts the force exerted on the optic nerve head is greatly increased compared to the young eye. Severing some of the posterior attachments in aging eyes restores some of the contractile mobility. This constellation of findings may have enormous implications with regard to the pathophysiology and treatment of not only presbyopia but also primary open angle glaucoma because of the alterations in stretch forces on the optic disc, where all one million of the optic nerve fibers meet to leave the eye and head for the brain.