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Nitric Oxide Synthase
Background & Summary of Research
Most treatment for glaucoma tries to lower pressure in the eye to stop or slow damage to cells and to save sight. The GRF-funded Collaborative Normal Tension Glaucoma Study, published in the American Journal of Ophthalmology in October 1998, showed that for most people, lowering pressure truly does slow down the progression of the disease.
However, there were 12% of people who still had continuing damage to their optic nerves, even with lower pressure. A study published in the Proceeding of the National Academy of Sciences on August 17, 1999 may help researchers find an answer for these people who still lose sight even though their eye pressure is lowered.
A drug called “aminoguanidine” was used on rats with high eye pressure. The researchers put the drug in the drinking water of some of the rats with high eye pressure, and others were not treated at all. After six months, the researchers found that the untreated rats lost 36% of their retinal ganglion cells in their eyes. The rats that got the drug “aminoguanidine” lost less than 10% of their retinal ganglion cells.
Aminoguanidine works by inhibiting the activity of an enzyme which makes nitric oxide in excess. This enzyme, nitric oxide synthase, has been found to be present in the optic nerve tissue of patients with glaucoma.
This means that there may be some treatment for glaucoma that will protect the optic nerve from damage, even if eye pressure cannot be controlled, or for those people who still have damage when pressure is controlled.
More research will be done in this area, with potential human trials if it is successful.
An abstract or full text of the article and reprint requests can be found at the National Academy of Sciences website.