Optic neuropathies and retinal ganglion cell death

Abstract

Retinal ganglion cells (RCG) may die through a variety of mechanisms. Optic atrophy is a nonspecific histological characterization of RGC axonal death by any means. Injury to RGC axons will usually lead to anterograde degeneration (towards the brain) and retrograde (back to the RGC) degeneration. Like all neurons, RGCs can die from either apoptosis or necrosis. Classical descriptions of chromotolysis refer to necrosis. Necrosis may be due to any injury that fully compromises the cell's vital functions. In contradistinction, apoptosis is programmed cell death. This carefully orchestrated series of intracellular events produces a quiet death that minimizes injury to adjacent cells. Extracellular signals for apoptosis may depend upon FAS ligand or several cytokines, particularly TNF. Strategies for neuroprotection may come from understanding and blocking either the intercellular signaling pathways or the intracellular cascades of events that lead to apoptosis.