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Abstract #14229 Published in IGR 8-3
Understanding optic nerve degeneration: Key to neuroprotection in glaucoma
Ferrer E; Bozzo JDrugs of the Future 2006; 31: 355-363
Glaucoma is a group of neurodegenerative disorders characterized by degeneration of optic nerve axons and retinal ganglion cell death. While the most common strategy in glaucoma therapy is aimed at lowering elevated intraocular pressure (IOP), an emerging field of research is currently focused on protecting the optic nerve from degeneration. Neuroprotection is directed at preventing or slowing the death of retinal ganglion cells, thereby decreasing the progression of visual field loss. In all optic neuropathies including glaucoma, the initial site of injury are the axons of retinal ganglion cells. Axonal injury triggers apoptotic mechanisms that ultimately culminate in retinal ganglion cell death. Neuroprotective approaches are varied: 1) the prevention of apoptosis by inhibiting TNF-α and caspase activity; 2) blocking excessive Ca2+ overload due to overactivation of NMDA receptors; or 3) blocking nitric oxide toxicity. Axonal injury may cause the blockade of retrograde axoplasmic transport of neurotrophins essential for retinal ganglion cells. In this sense, neurotrophic factors such as brain-derived neurotrophic factor (BDNF) have been reported to prolong retinal ganglion cell survival, and α2 -adrenoceptor agonists such as brimonidine are thought to exert their neuroprotective effects partly by upregulating BDNF expression. Modulation of the immunological response has also proved effective in reducing retinal ganglion cell loss, suggesting a possible use of vaccines to prevent glaucoma progression.
Dr. E. Ferrer, Prous Science, P.O. Box 540, Barcelona 08080, Spain
Classification:
11.8 Neuroprotection (Part of: 11 Medical treatment)
