Molecular and cell-based approaches for neuroprotection in glaucoma

Optom Vis Sci. 2008 Jun;85(6):417-24. doi: 10.1097/OPX.0b013e31817841f7.


A hallmark of glaucomatous optic nerve damage is retinal ganglion cell (RGC) death. RGCs, like other central nervous system neurons, have a limited capacity to survive or regenerate an axon after injury. Strategies that prevent or slow down RGC degeneration, in combination with intraocular pressure management, may be beneficial to preserve vision in glaucoma. Recent progress in neurobiological research has led to a better understanding of the molecular pathways that regulate the survival of injured RGCs. Here we discuss a variety of experimental strategies including intraocular delivery of neuroprotective molecules, viral-mediated gene transfer, cell implants and stem cell therapies, which share the ultimate goal of promoting RGC survival after optic nerve damage. The challenge now is to assess how this wealth of knowledge can be translated into viable therapies for the treatment of glaucoma and other optic neuropathies.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Apoptosis
  • Brain-Derived Neurotrophic Factor / genetics
  • Brain-Derived Neurotrophic Factor / physiology
  • Glaucoma / drug therapy*
  • Glaucoma / genetics*
  • Glaucoma / pathology
  • Glaucoma / physiopathology
  • Humans
  • Nerve Growth Factors / genetics
  • Nerve Growth Factors / physiology
  • Neuroprotective Agents / therapeutic use*
  • Optic Nerve / pathology
  • Retinal Ganglion Cells / pathology
  • Signal Transduction
  • Stem Cell Transplantation


  • Brain-Derived Neurotrophic Factor
  • Nerve Growth Factors
  • Neuroprotective Agents