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The glaucomas are a group of eye diseases characterized by progressive ganglion cell and optic nerve damage, leading to constriction of the visual fields and eventual loss of central vision. Although the disease is typically associated with increased intraocular pressure (IOP), there are patients with low- or normal-tension glaucoma and others with elevated IOP who do not experience optic nerve damage. The ocular pathology observed in glaucoma can affect the trabecular meshwork (TM; the main outflow tract for intraocular fluid), the ganglion cell layer of the retina, and the optic nerve head and associated lamina cribrosa. Therapies for these diseases have largely been directed at lowering IOP through pharmacologically decreasing aqueous humor production in the ciliary body or increasing outflow by targeting the TM with drugs or surgical intervention. Although these approaches can lead to significant lowering of the IOP, most patients still experience progressive visual loss, albeit at a slower rate than occurs if the high pressure is left untreated. More recently, efforts have been directed at providing neuroprotection for the cells primarily responsible for vision loss, the retinal ganglion cells (RGCs). Recent advances in stem cell biology, regenerative medicine, and cell-based therapies provide the opportunity to protect or replace cells damaged by increased IOP or other less well-understood abnormalities associated with glaucoma. In this article, I review recent advances in the areas of stem cell biology and cell-based delivery of neuroprotectants for the treatment of retinal diseases and discuss their potential applications for the treatment of glaucoma. I also review recent advances in metabolomics and transcriptomics that will enable analysis of factors that may be present in patients who have increased IOP but no damage from glaucoma.
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Martin Friedlander (2012) studied this question.
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