Glaucoma represents a group of neurodegenerative diseases characterised by structural damage to the optic nerve and slow, progressive death of retinal ganglion cells (RGCs). Elevated intraocular pressure is traditionally considered to be the most important risk factor for glaucoma, and treatment options for the disease have hitherto been limited to its reduction. However, visual field loss and RGC death continue to occur in patients with well controlled intraocular pressures and, thus, a consensus has recently emerged that additional treatment strategies are needed. One such strategy is pharmacological neuroprotection, which in the context of glaucoma, refers to the situation in which a drug is deployed to interact with neuronal or glial elements within the retina/optic nerve head and thereby facilitate the survival of RGCs. The advent of animal models of chronic glaucoma has enhanced our understanding of many of the pathological processes occurring in glaucoma and, in doing so, described logical targets for pharmacological intervention. Such targets, which have been manipulated with varying degrees of success in relevant animal paradigms include glutamate receptors, autoimmune elements, neurotrophin deprivation, nitric oxide synthesis, oxidative stress products, sodium and calcium channels, heat shock proteins and apoptotic pathways. With exciting data now emerging from many research laboratories, it is obvious that pharmacological neuroprotection for glaucoma without doubt represents an exciting development in the search for a treatment modality for this debilitating disease.