Purpose To present hypotheses and their supportive evidence that neuroprotective therapies could supplement eye pressure lowering in the treatment of glaucoma. Methods. Studies of histological and physiological behavior of retinal ganglion cells in experimental models of glaucoma in monkey and rat, as well as in human glaucoma eyes. Results In glaucoma, ganglion cells are injured at the optic nerve head, where anterograde and retrograde axonal transport is blocked. Evidence will be presented that transport of receptors carrying certain neurotrophins is blocked in experimental glaucoma. Support for apoptosis of ganglion cells in experimental and human glaucoma will be given. It has been shown that delivery of neurotrophins delays ganglion cell apoptotic death after experimental optic nerve injury. Conclusions Some cell death in glaucoma represents suicide generated by activation of genetic programs, hypothetically due to low levels of neurotrophins at the cell body. Delivery of neurotrophins or repression of apoptosis by somatic genetic manipulation of ganglion cells in vivo may offer protection from cell death. This approach is potentially applicable to other optic neuropathies characterized by retrograde degeneration.
|Original language||English (US)|
|Journal||Investigative Ophthalmology and Visual Science|
|State||Published - Dec 1 1997|
ASJC Scopus subject areas
- Sensory Systems
- Cellular and Molecular Neuroscience