The causes of glaucoma are complex and so are its treatment regimens. It is almost as if glaucoma were several separate diseases. Controlling intraocular pressure (IOP) in the anterior segment is certainly a prime consideration, but the pathologic endpoint of glaucoma is the death of the retinal ganglion cell in the posterior segment. The disease itself is probably best called an optic neuropathy, one of many diseases that can affect neuronal cells. However, it is unique as to the cell affected (the ganglion cell) and the endpoints of the disease process. Biologically and physically, glaucoma is characterized by changes in the optic disc, optic nerve, and brain and by ganglion cell death. Functionally, the changes lead to visual impairment, as best exemplified by a decrease in visual field. Thus, developing methods of preserving ganglion cell function and lifespan are the ultimate goals in maintaining vision in glaucoma. One way to achieve preservation is through neuroprotection—the use of neuron-survival (neurotrophic) agents. In a rational approach to disease control, one should first ask: What are the stages of glaucoma pathology where neurotrophic agents might be effective? Probably not at the stage of an initial insult or injury such as with a genetic mutation, increased IOP, and so on. Intervention can come relatively early, though, maybe at the first signs of physical and structural changes in the disc region and optic nerve, or at least at the first signs of vision loss. These changes would be rooted in biochemical alterations secondary to the primary insult but still early enough to slow, halt, or even reverse the disease process. A prime therapeutic target would be the process of cell death of the ganglion cells; similarly, a secondary target would be the induced degeneration to neighboring ganglion cells through a “bystander” effect. An important but difficult area would be controlling gliosis and the changes that occur in glial activation. However, the effects of neurotrophic agents will be different at different stages of the disease, with obviously no effect after most or all the ganglion cells are dead.