title: Neuroprotection in glaucoma--delusion, reality or hope?
abstract: The global definition of glaucoma considers it as an optic neuropathy with multifactor etiology, which affects the optic nerve head (ONH), provoking visual field loss and permanent impairment of visual function. Bearing in mind the fact that the exact pathogenic mechanism is still not completely established, glaucoma treatment strategies so far are based upon the identification of glaucoma risk factors. Among them, only elevated intraocular pressure (IOP) could undergo therapeutic treatment. However, in spite of the adequate therapy and IOP lowering, very often the disease is still progressing, leading to definite visual loss and permanent blindness. This especially refers to "normal tension glaucoma". Over the last decade, there has been significant scientific research on new strategies for the delay or prevention of retinal ganglion cell loss (RGC), which is the basic pathophysiological event that initiates the cascade of processes leading to optic atrophy. Therefore, a great deal of expectation has been put on the concept of what is known as "neuroprotection". This includes the development of treatment strategies (pharmacological, immunological, genetic) that would be capable of preventing apoptotic death of retinal ganglion cells. The concept of neuroprotection is based upon increasing evidence that glaucoma degeneration is analogous with other neurodegenerative diseases of the central nervous system suggesting a strong relation between the basic cellular processes in glaucoma and Alzheimer's disease, for example. It is considered that retinal ganglion cell death goes through two phases--primary injury responsible for initiation of damage that is followed by slower secondary degeneration related to a harmful environment surrounding the degenerated cells. Neuroprotection in glaucoma refers to any intervention that is aimed at prevention of the optic nerve head injury and ganglion cells death. Pharmacological intervention is aimed at neutralizing some of the effects of the nerve-derived toxic factors by increasing the ability of the remaining neurons to cope with stressful conditions. On the other hand, immunological reaction stimulates the body's repair mechanisms so as to hinder the toxic effects of various chemical agents generated during pathological events.
authors: University Eye Diseases Clinic, Skopje, R. Macedonia.
authors: A
authors: A
authors: Dimovska-Jordanova
mesh_terms: D017209:Apoptosis; D019610:Cytoprotection; D015316:Genetic Therapy; D005901:Glaucoma / Q000503:physiopathology / Q000517:prevention & control*; D018696:Neuroprotective Agents / Q000627:therapeutic use*; D012165:Retinal Ganglion Cells / Q000187:drug effects*
chemical_list: D018696:Neuroprotective Agents