Neuroprotection in glaucoma: A model for nouroprotection in optic neuropathies

Tania Sibila Marcic, David Anthony Belyea, Barrett Katz

Research output: Contribution to journalReview article

34 Scopus citations

Abstract

Purpose of review: Efforts to discover modalities and pathophysiologies that might afford successful neurorescue, neurorestoration, and neuroprotection of cells of the central nervous system have focused on processes that affect the central nervous system proper, that is, the brain. Often overlooked in the search for neural protection is the fact that the mammalian optic nerve behaves in many ways as an integral part of the central nervous system. As such, the eye-the optic nerve and retina-affords an ideal clinical model for neuroprotection and neuroprotective agents. Glaucomatous optic neuropathy is the most prevalent of all adult optic neuropathies, and offers an ideal primate and lower mammalian animal model for investigations of neuroprotection. Recent findings: This is especially compelling because while recent studies in glaucoma have shown reduction of intraocular pressure (IOP) to be an effective modality in the treatment of glaucomatous opt c neuropathy, not all patients respond to or can achieve meaningful IOP reductions. Therefore much attention has now been focused on neuroprotection as a strategy in therapies for glaucomatous optic neuropathy as a means of preserving retinal ganglion cells and their axonal projections. Summary: This review discusses the latest studies on various mechanisms of neuroprotection in the treatment of glaucomatous optic neuropathy.

Original languageEnglish (US)
Pages (from-to)353-356
Number of pages4
JournalCurrent opinion in ophthalmology
Volume14
Issue number6
DOIs
Publication statusPublished - Dec 1 2003

    Fingerprint

Keywords

  • Apoptosis
  • Axon
  • Glaucoma
  • Neurodegeneration
  • Neuroprotection
  • Neurorepair
  • Neurorescue
  • Neurorestoration
  • Optic nerve
  • Retinal ganglion cell

ASJC Scopus subject areas

  • Ophthalmology

Cite this