BY EVE JACOBS
T
he retina is a delicate structure at the back of the eye that is critical to vision. Damage to this light-sensing tissue can impede the exquisitely orchestrated flow of light and image from lens to brain that we call sight. Some changes to the retina so severely impair eyesight that they are life-changing, for sure. For Robert Wigder that life-changing news came like a one-two punch between the eyes. First, in June 2006, he was diagnosed with dry age-related macular degeneration (AMD) — requiring his eye condition to be monitored biannually. Then in July 2007, he was diagnosed with the wet form of AMD, also known as choroidal neovascularization. The difference between the two remains a huge mystery to most people — but, in fact, they are quite different in terms of symptoms, progression and treatment. For Marco Zarbin, MD, PhD, the details of the macula and its range of damaging changes are crystal clear. But a drive to understand how to halt those changes and then reverse them — ultimately restoring lost sight— is the impetus that drives his arduous research forward year by year. Zarbin is chair of the Institute of Ophthalmology and Visual Science (IOVS) at NJMS, where he oversees all aspects of the Institute’s life, including exceptionally busy clinical practices, a highly regarded residency program in ophthalmology (the only one based in the state), outreach to underserved members of the Newark community and its environs that has changed the eye-care picture for many local residents, and research— both lab-based and clinical trials — that helps develop new and better therapies. Zarbin himself has earned a far-reaching reputation as an expert in diagnosing and treating retinal disease, as well as actively pursuing research in AMD. First, a short explanation is in order. AMD is a degenerative disease that tends to affect those older than 60 and involves the macula (the small central portion of the retina) that supports fine vision, which is needed to read, recognize faces, and drive. The dry form of the disease is diagnosed when yellow deposits, called drusen, form under the macula. As the deposits, which are thought to be abnormal accumulations of cellular debris, grow in size and multiply, they can cause vision to dim or be distorted. As the disease advances, the light-sensitive layer of cells (called photoreceptors) in the macula can die, as can cells called retinal pigment epithelium (RPE) that partner with photoreceptors to 28
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support vision. As a result of photoreceptor and RPE death, patients can develop blind spots in the center of their vision, and eventually lose central vision. This advanced form of dry AMD is called geographic atrophy. The dry form is much more common than the wet AMD. “Dry macular degeneration sometimes leads to the wet form,” Zarbin states. “How the dry form of AMD progresses to the wet form is not known exactly, nor is it understood why some patients never progress to geographic atrophy, why some patients with early AMD never progress to the wet form of the disease, or why some patients develop both geographic atrophy and choroidal neovascularization,” he continues. Only about 10 percent of those with AMD develop the more damaging wet form of the disease in which abnormal blood vessels grow under the macula and leak blood and fluid into the retina. Blind spots, loss of central vision, and distortions, such as straight lines appearing wavy, can result from dysfunction and death of the lightsensitive retinal cells. The wet form is treatable with drugs (and other therapies) that often halt its progression but do not cure or reverse the disease. As a result, patients with wet AMD still can lose central vision despite treatment. For Wigder, the bad news of his diagnosis with the wet form of AMD was followed by the good news that a drug called ranibizumab — which received FDA approval in 2006 — would likely slow down the disease’s progression. It is a form of a colorectal cancer drug called bevacizumab that inhibits a protein (vascular endothelial growth factor) known to stimulate the growth of new abnormal blood vessels. For Wigder, the thought of a monthly injection into the eye was horrific, but the potential loss of vision was even more frightening. He needed a lot of hand-holding to get through the first treatments, he admits, but that’s exactly what he got at IOVS. Wigder is not by nature a fearful man. In 1959, he founded Wigder Chevrolet in Livingston, and he has built his business from the ground up. He now employs more than 50 people and is still an active and vital part of the enterprise. That is germane to this story for two reasons. First and foremost, he’s not ready to give up his professional life, and he very much needs his vision to stay actively involved. Secondly, he has a deep appreciation JOHN EMERSON
