Weizmann Institute scientists have succeeded in stopping the progressive loss of eyesight in animals with a glaucoma-like disease. Their innovative study, reported in the March 6, 2001 issue of the Proceedings of the National Academy of Sciences U.S.A., suggests that Copaxone, a drug developed at the Weizmann Institute of Science to treat multiple sclerosis, may also stop, or at least slow down, the loss of eyesight in people with chronic glaucoma.
Glaucoma, which affects 1 percent of the adult population, is the main cause of blindness in adults. The majority of patients with chronic glaucoma have increased pressure inside the eye due to defective drainage of the transparent fluid that bathes the eye and nourishes its outer cells. The increase in this intraocular pressure (IOP) damages the optic nerve, causing it to degenerate and often leading to loss of eyesight.
For many years, the search for improved glaucoma therapies focused on correcting the eyes drainage system to reduce IOP. Eventually, however, it became clear that reducing the pressure was not enough to halt the ongoing degeneration of the optic nerve and did not eliminate the risk of blindness. Scientists concluded that a crucial factor was being overlooked and they set out in search of this missing link.
Approximately five years ago, Prof. Michal Schwartz of the Weizmann Institutes Neurobiology Department proposed a new concept to account for the continuing degeneration of the optic nerve that occurs after the pressure in the eye had been reduced. Schwartz suggested that while the initial damage to the optic nerve is indeed caused by increased eye pressure, secondary factors triggered by the initial damage contribute to the nerve's ongoing degeneration.
The offending factors include chemicals that play an important role in the life of a healthy nerve, but when the nerve degenerates, their concentrations increase to a toxic level. One of these chemicals i
Contact: Jeffrey Sussman
American Committee for the Weizmann Institute of Science