Weizmann Institute scientists have succeeded in stopping the progressive loss of eyesight in animals with a glaucoma-like disease. Their innovative study, reported a recent 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.
For many years, the search for improved glaucoma therapies focused on correcting the eye's drainage system to reduce the disease. Eventually, however, it became clear that reducing the pressure was not enough to halt the degeneration of the optic nerve. About five years ago, Prof. Michal Schwartz of the Weizmann Institute's Neurobiology Department proposed a new concept to account for the continuing degeneration of the optic nerve. She suggested that while the initial damage to the optic nerve is caused by increased eye pressure, secondary factors triggered by the initial damage contribute to the nerve's ongoing degeneration. She believed that the neurotransmitter glutamate, which spills from damaged nerve cells and adversely affects healthy neighboring cells, had an impact on vision loss. Her research ultimately led her to demonstrate that immunization with the drug Copaxone protects the damaged optic nerve from neuronal degeneration. For more details on the study, see http://wiswander.weizmann.ac.il/weizmann/doa_iis.dll/Serve/item/English/1.200.7.2.html
For many years, the search for improved glaucoma therapies focused on correcting the eye's drainage system to reduce the disease. Eventually, however, it became clear that reducing the pressure was not enough to halt the degeneration of the optic nerve. About five years ago, Prof. Michal Schwartz of the Weizmann Institute's Neurobiology Department proposed a new concept to account for the continuing degeneration of the optic nerve. She suggested that while the initial damage to the optic nerve is caused by increased eye pressure, secondary factors triggered by the initial damage contribute to the nerve's ongoing degeneration. She believed that the neurotransmitter glutamate, which spills from damaged nerve cells and adversely affects healthy neighboring cells, had an impact on vision loss. Her research ultimately led her to demonstrate that immunization with the drug Copaxone protects the damaged optic nerve from neuronal degeneration. For more details on the study, see http://wiswander.weizmann.ac.il/weizmann/doa_iis.dll/Serve/item/English/1.200.7.2.html