Sarfarazi is a professor of genetics. He directs the Surgical Research Center at the UConn Health Center. According to peers and fellow researchers from Toronto, Chicago and New York, he is among the top experts in the world on the genetics of glaucoma. This February, together with research associate Tayebeh Rezaie, he pinpointed the cause of primary open-angle glaucoma (POAG), a leading cause of blindness. Their findings first appeared in Science.

POAG can lie in wait for as long as 30 years, producing few or no symptoms. Then it blindsides victims, leaving them with the classic tunnel vision symptomatic of glaucoma. Detected too late, blindness is inevitable -- but sight loss can be limited if the disease is diagnosed early. Suspecting that POAG has genetic roots, Sarfarazi set out to find a genetic marker to use in detecting the disease.

The research team found it by meticulously studying 54 families with inherited, adult-onset glaucoma. In a significant number of these patients, a specific gene sequence on one chromosome was damaged by mutations. The researchers learned that one of the genes in the sequence gives instructions for a special eye protein they named "optineurin."

Normal optineurin suppresses a devious protein that kills optic nerve cells prematurely. Sarfarazi theorizes that in patients diagnosed with POAG, mutated optineurin can't perform this task. Peripheral vision narrows, and eventually vision is squeezed to the zero point.

Now that he has pinpointed the mutation, he and Rezaie hope to develop a drug that can reverse its effects. In the meantime, the discovery can help doctors diagnose POAG years in advance of symptoms, so patients can be treated and eyesight loss deferred and curbed.

The research continues Sarfarazi's life interest in how the optic nerve interacts with the brain. For people who don't yet know that POAG is their genetic fate, it could remove a major blind spot -- for Sarfarazi and his team, that makes the years of disciplined effort worth every second.