Abstract: The present invention provides a method for treating or reducing damage to the optic nerve in a subject comprising administering to the subject a therapeutically effective amount of prostaglandin J2 alone or in combination with an effective amount of GM-CSF. In particular aspects of the invention, the subject is a mammal, and in further aspects the mammal is a human.

Abstract: The present invention provides a method for treating or reducing damage to the optic nerve in a subject comprising administering to the subject a therapeutically effective amount of prostaglandin J2 alone or in combination with an effective amount of GM-CSF. In particular aspects of the invention, the subject is a mammal, and in further aspects the mammal is a human.

Abstract: Anterior ischemic optic neuropathy is an ischemic disease affecting the optic nerve. A blockage of vessels supplying the intra-retinal portion of the optic nerve causes loss of axon transport stasis, retinal ganglion cell, specific dysfunction, and RGC death. Research has been limited by the lack of low-cost models for this disease. Using a custom contact lens, an intravenous injection of photosensitizing agent anesthetizes male Sprague-Dawley rats. A laser activate dye within the small vessels perfusing the optic nerve. This treatment spared the larger vessels perfusing the inner retina. Electropliysiologically, a decrease in amplitude of the visual evoked potential is noted. Histologically, alterations in axonal transport are seen. Reverse-transcriptase based Polymerase chain later retinal gene expression changes in treated animals. This method replicates many cellular and molecular level changes in a low-cost animal model.

Abstract: Anterior ischemic optic neuropathy (AION) is one of a family of ischemic diseases affecting the optic nerve. A blockage of vessels supplying the intra-retinal portion of the optic nerve results in loss of axon transport stasis, retinal ganglion cell (RGC)—specific dysfunction, and RGC death. AION research has been limited by the lack of a low-cost model for this disease. The invention of such a model has now been developed. Using a custom contact lens, an intravenous injection of photosensitizing agent is administered to anesthetize male Sprague-Dawley rats. A laser was used to activate dye within the small vessels perfusing the optic nerve. This treatment was adjusted to spare the larger caliber vessels perfusing the inner retina. Electrophysiologically, a decrease in amplitude of the visual evoked potential is noted. Histologically, alterations in axonal transport are seen.