|
|
||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
SYMPOSIUM REPORT |
1 Department of Physiology
2 The Neuroscience Program, Michigan State University, East Lansing, MI, USA
3
Indiana University School of Optometry, Bloomington, IN, USA
Glaucoma is an optic neuropathy that originates with pressure-induced damage to the optic nerve. This results in the retrograde degeneration of ganglion cells in the retina, and a progressive loss of vision. Over the past several years, a number of studies have described the structural and functional changes that characterize ganglion cell degeneration in the glaucomatous eye, and following optic nerve injury. In addition, a variety of different strategies for providing neuroprotection to the injured retina have been proposed. Many of these are based on the use of brain-derived neurotrophic factor (BDNF), a particularly potent neuroprotectant in the mammalian eye and the basis of our research in this area. Of particular importance is the fact that BDNF not only promotes ganglion cell survival following damage to the optic nerve, but also helps to preserve the structural integrity of the surviving neurons, which in turn results in enhanced visual function. The studies presented here describe these attributes, and serve as the foundation for ongoing work that suggests a need to think beyond the eye in the development of future treatment strategies.
(Received 12 May 2008;
accepted after revision 16 June 2008;
first published online 19 June 2008)
Corresponding author A. J. Weber: Department of Physiology, Michigan State University, East Lansing, MI 48824, USA. Email: weberar{at}msu.edu
This article has been cited by other articles:
![]() |
Z. J. Zhou and M. A. McCall Retinal ganglion cells in model organisms: development, function and disease J. Physiol., September 15, 2008; 586(18): 4343 - 4345. [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |