Abstract
The goal of neuroprotection in glaucoma treatment is to employ agents that prevent or delay apoptosis of retinal ganglion cells (RGC) and facilitate regeneration of already damaged calls. The following contribution discusses the mechanisms of RGC death and current status of neuroprotective in vivo studies and investigations on cell cultures and animal models. Discussions on the etiopathogenesis of PCOAG center on elevated IOP and ocular disorders of vascular function. The mechanisms of axonal damage induced by ischemia are explained and the resultant possible neuroprotective effect mechanisms are discussed (Na(+) or Ca(2+) channel blockers, role of reactive astrocytes). Substitution of axonal survival factors and especially the role of BDNF are described. Glutamate excitotoxicity also plays a role in glaucomatous antegrade RGC death. Relevant questions and possible therapeutic approaches are discussed. The three phases of apoptosis cascade and the key role of mitochondria in the insult-induced apoptosis are considered as well as the still relatively unexplored possibilities of RGC regeneration. Finally, perspectives of neuroprotective treatment of PCOAG are presented.
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