[Mechanisms of neuroprotection against glaucoma]

Ophthalmologe. 2004 Nov;101(11):1076-86. doi: 10.1007/s00347-004-1130-1.
[Article in German]

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.

Publication types

  • English Abstract
  • Review

MeSH terms

  • Animals
  • Apoptosis / drug effects
  • Glaucoma, Open-Angle / complications
  • Glaucoma, Open-Angle / drug therapy
  • Glaucoma, Open-Angle / metabolism*
  • Humans
  • Nerve Degeneration / etiology
  • Nerve Degeneration / metabolism
  • Nerve Degeneration / prevention & control
  • Neuroprotective Agents / therapeutic use*
  • Neurotransmitter Agents / metabolism*
  • Retinal Degeneration / etiology
  • Retinal Degeneration / metabolism*
  • Retinal Degeneration / prevention & control
  • Retinal Ganglion Cells / drug effects
  • Retinal Ganglion Cells / metabolism*
  • Retinal Ganglion Cells / pathology

Substances

  • Neuroprotective Agents
  • Neurotransmitter Agents