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What are the key research accomplishments from the eight years that the Catalyst For a Cure has studied glaucoma?
I can group them into two major findings:
As a group, the Catalyst For a Cure research team was able to show that the primary cell that’s affected in glaucoma, the retinal ganglion cell, does not die early in the stages of the disease. Its death is quite delayed in the disease process.
Why that’s important is that we showed that there are many changes in that retinal ganglion cell that are akin to what you see in other neurodegenerative diseases.
Since we now know that the progressive degenerative process is very slow, this has really changed the way the field thinks that we should target the disease.
We’ve discovered that early changes in the ganglion cell undergo a degenerative process long before the cell itself begins to die.
We are now thinking about how to prevent or slow this process enough to slow the progress of the disease and thereby preserve vision for a person’s lifetime.
While clinicians and scientists have thought of glaucoma as a ganglion cell disease, our group has shown that glaucoma is not a “cell autonomous” disease - some of the latest data suggests that other cells in the retina are equally affected or equally contribute to the rate and decline of the ganglion cells.
This is exciting because it gives us other targets to intervene. These other cell types are very important in the function and support of the ganglion cell.
Thinking of glaucoma as a retinal degenerative disease, and looking at the pathways of these other cells and how they may contribute, gives us a broadened target for intervention. This is very important - a key understanding in the way neurodegeneration occurs.
This data suggests that there may be “master programs” for degeneration. I predict we will find that there are programs that link all these cells together, that when a cell is under stress it is communicating with these other cell types, leading to degeneration.
Because it’s a master program, there has to be a coordinator. Once we can find the coordinator of all these systems, we should be able to intervene and “turn off” that program.
That’s pretty exciting, because if you could find the “coordinator” and change or turn off the program, that would be a way to potentially stop the degeneration and save vision.
Yes, that's right.
The Catalyst For a Cure consortium has helped us to understand that glaucoma is part of a family of neurodegenerative diseases. What are the implications of these findings for other neurodegenerative diseases, like Alzheimer’s or Parkinson’s?
There is some exciting new data coming out from studies of other neurodegenerative diseases, and that data is similar to what we are finding in glaucoma.
For example, Parkinson’s disease, as well as ALS, were thought to be neuronal diseases; just recently it was shown in Parkinson’s disease that you can manipulate a gene in the supporting cell around the neurons, and that if you stimulate a specific stress pathway in the support cells, you can dramatically slow down the progression of the disease.
We’ve noted that this same pathway is prevalent in glaucoma, and we’ve shown that these support cells are activated very early in glaucoma. We’re very excited about this concept, that maybe it’s the same molecular pathway that leads to degeneration in multiple neurodegenerative diseases.
These exciting discoveries and breakthroughs show us that a cure is possible, and that we’re closer than ever, but there is still work to do before glaucoma can be a thing of the past. With the continued generous support of the community, and your commitment to getting involved, we can turn these breakthroughs into action, and that action into a cure.
This article is excerpted from a May 14, 2009 GRF President’s Teleconference with members of our Catalyst Circle, in which Philip Horner, PhD of the University of Washington reports on recent discoveries by the Catalyst For a Cure research consortium.
Last reviewed on August 02, 2016
This article appeared in the September 2009 issue of Gleams.Subscribe