[PDF][PDF] Retinal ganglion cell death in glaucoma: mechanisms and neuroprotective strategies.

MH Kuehn, JH Fingert, YH Kwon - development, 2005 - myweb.uiowa.edu
development, 2005myweb.uiowa.edu
Neuroprotection can be defined as any therapeutic paradigm designed to prevent or delay
neuronal cell death and maintain neural function. In glaucoma, progressive death of the
retinal ganglion cells (RGCs) leads to optic nerve degeneration and, ultimately, vision loss.
The aim of glaucoma therapy is, therefore, to facilitate the survival of RGCs. Currently,
glaucoma treatment relies on pharmacologic or surgical reduction of intraocular pressure
(IOP). Ample evidence shows that reducing IOP provides effective neuroprotection against …
Neuroprotection can be defined as any therapeutic paradigm designed to prevent or delay neuronal cell death and maintain neural function. In glaucoma, progressive death of the retinal ganglion cells (RGCs) leads to optic nerve degeneration and, ultimately, vision loss. The aim of glaucoma therapy is, therefore, to facilitate the survival of RGCs. Currently, glaucoma treatment relies on pharmacologic or surgical reduction of intraocular pressure (IOP). Ample evidence shows that reducing IOP provides effective neuroprotection against the demise of RGCs in glaucoma [1–3].
The development of animal models of glaucoma has allowed investigation into the cellular and molecular mechanisms of this disease. Experimental elevation of IOP animal models of glaucoma induces structural, biochemical, and functional changes that resemble those of the disease in humans, including disorganization and compositional changes in the optic nerve head (ONH), RGC apoptosis, and visual deficits [4–10]. This article describes the cellular mechanisms of RGC death in glaucoma and the emerging neuroprotective strategies that are based on these mechanisms.
myweb.uiowa.edu