Dr. Joel S. Schuman

Dr. Joel S. Schuman

Tufts ophthalmologist honored for groundbreaking research

The New York Academy of Medicine has awarded the 2002 Lewis Rudin Glaucoma Prize to two trailblazing ophthalmology researchers who have discovered a molecular mechanism behind glaucoma, the world's leading cause of irreversible blindness.

Dr. Joel S. Schuman, professor of ophthalmology at Tufts School of Medicine and director of the Glaucoma Service at the New England Eye Center at Tufts-New England Medical Center, and M. Elizabeth Fini, professor and co-director of research at the Bascom Palmer Eye Institute at the University of Miami School of Medicine, will share the $50,000 Rudin Prize.

Schuman and Fini are being honored for their March 2001 research paper, published in Nature Medicine, in which they identify the first-ever molecular marker for human glaucoma. They examined normal and glaucoma-stricken eyes from cadavers and found that a certain molecule—ELAM-1—was detectable only in the ailing eyes. Nan Wang and Shravan K. Chintala were also authors on the paper.

In an article accompanying the research, Stanislav Tomarev of the National Eye Institute hailed the discovery as a critical step in improving future detection and treatment of glaucoma. The eye disease has no symptoms and surreptitiously steals a person's vision. As many as half of those with early-stage glaucoma do not realize they have it, making early detection a vital tool. It affects more than three million adults in the United States and 17 million worldwide.

"We found there was a fundamental molecular difference between people who have glaucoma and people who don't," said Schuman, who also is an adjunct professor in Tufts' School of Engineering. "If we can use this finding to develop a diagnostic test, it may allow us to identify people who have glaucoma better than we can now."

Fini and Schuman are conducting follow-up studies into treatments for glaucoma, including an investigation into whether glaucoma patients have genetic abnormalities that might lead to over-expression of ELAM-1.

Many cases of glaucoma occur because the eye's optic nerve is damaged by the build up of aqueous humor fluid in the eyes. Under normal conditions, this fluid circulates between the front and back chambers of the eye, nourishing the lens and corneal cells. It then drains through the trabecular meshwork tissue and flows out into the Schlemm's canal. When these two parts don't function properly, drainage is impaired, and pressure builds up on the optic nerve. The researchers found that the ELAM-1 molecule (short for endothelial leukocyte-adhesion molecule-1) was over-expressed in these two parts of glaucoma-stricken eyes.

They also found that the ELAM-1 protein was consistently present in cell lines derived from the trabecular meshwork tissue of glaucomatous eyes, but not present in the same tissue in normal eyes. Combined, the findings identify ELAM-1 as the first true molecular tag for glaucoma.

Interestingly, Schuman and Fini also discovered that ELAM-1 is actually part of a stress response that protects cells and tissues in the eyes' outflow pathways. They theorize that this protective response leads to eye tissue damage if it continues on a chronic basis. That tissue damage leads to the pressure build up that is characteristic of glaucoma.

The researchers are now working to understand the dynamics of this helpful-to-harmful change in the hope of devising a way to reverse it. "Characterizing the change could provide us with potential new targets for drug therapy," said Fini.

This research was deemed so significant that it was published as the cover story in Nature Medicine. An abstract of the paper was printed in the journal Nature—something reserved for only the most significant research findings.

The New York Academy of Medicine awards the Rudin Prize for the most significant glaucoma research published in the prior year.