Axonal loss and neuroprotection in optic neuropathies

Can J Ophthalmol. 2007 Jun;42(3):403-8.

Abstract

Most optic neuropathies do not have effective treatments. Examples are ischemic optic neuropathy, Leber hereditary optic neuropathy, optic neuritis, and traumatic optic neuropathy. In some cases, the pathophysiology of the optic nerve injury is not fully understood. For example, while the demyelinative aspects of optic neuritis have been studied, the mechanism by which the axonal loss occurs is less apparent. In other cases, although the pathophysiology of the optic neuropathy may be understood, there is difficulty treating the disease, for example, with traumatic optic neuropathy. In response to this therapeutic dearth, the concept of neuroprotection has arisen. Neuroprotection is a therapeutic paradigm for preventing death of neurons from injury and maintaining function. In optic neuropathies, the corresponding neuron is the retinal ganglion cell. These cells are unable to divide, and optic neuropathies irrevocably result in their death; therefore, the primary target of neuroprotection are retinal ganglion cells and their axons. This review emphasizes that most optic neuropathies are axonal and thus good targets for neuroprotection.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Apoptosis / drug effects*
  • Axons / drug effects*
  • Axons / pathology
  • Humans
  • Neuroprotective Agents / therapeutic use*
  • Optic Nerve Diseases / pathology
  • Optic Nerve Diseases / prevention & control*
  • Retinal Ganglion Cells / drug effects*
  • Retinal Ganglion Cells / pathology

Substances

  • Neuroprotective Agents