Schwartz M, Belkin M, Yoles E, Solomon A
Department of Neurobiology, Weizmann Institute of Science, Rehovot, Israel.
J Glaucoma. 1996 Dec;5(6):427-32.
This article presents the rationale and an experimental strategy for the development of new treatment modalities for glaucomatous neuropathy. Accumulating evidence suggests that regardless of the primary trigger of the retinal and optic nerve damage in glaucoma, the disease will continue to progress even when the cause is removed. The resulting damage can be mimicked by the progression of damage secondary to an acute partial crush injury at the optic nerve head. Such secondary damage includes degeneration of the directly injured optic nerve fibers culminating in death of their cell bodies, as well as degeneration of nerve fibers that escaped acute injury but nevertheless deteriorate as a result of their exposure to injury-induced mediators of secondary degeneration released by the directly affected neurons.
We therefore propose that substances found to be effective in rescuing fibers from secondary degeneration and in increasing the survival rate or prolonging survival of retinal ganglion cells in the partially lesioned optic nerve may be useful for the treatment of glaucoma. The new approach does not replace hypotensive therapy, but addresses the glaucoma-induced damage by promoting nerve protection and neuroregeneration.
