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On September 17, 2020, Glaucoma Research Foundation presented an Innovations in Glaucoma Webinar, "Retinal Ganglion Cell Replacement: One step closer to vision restoration."
Watch the recorded webinar:
The 45-minute webinar features a presentation from Anna La Torre, PhD, a principal investigator in the Catalyst for a Cure research consortium funded by GRF. Dr. La Torre’s laboratory focuses on generating retinal ganglion cells from stem cells to enhance axonal growth and cell survival and ultimately, to use these cells as donor cells for cell replacement therapies and disease modeling.
Anna La Torre, PhD
Associate Professor, Department of Cell Biology and Human Anatomy, School of Medicine, University of California, Davis
Thomas M. Brunner
President and CEO, Glaucoma Research Foundation, San Francisco
Tom Brunner: Good afternoon. My name is Tom Brunner, and I'm the president and CEO of Glaucoma Research Foundation. This webinar is a special thank you to our donors for your support of Glaucoma Research Foundation and our mission to restore vision. Today's webinar is Retinal Ganglion Cell Replacement — One Step Closer to Vision Restoration. We'll hear about the Catalyst for a Cure Vision Restoration Initiative and their latest progress. Dr. Anna La Torre has very kindly agreed to join us today to talk about the incredible work she has been doing to help cure glaucoma.
Anna is a member of Glaucoma Research Foundation's Catalyst for a Cure team, together with Drs. Xin Duan, Yang Hu, and Derek Welsbie. Anna attended the University of Barcelona in Spain where she received a Master's in cell biology and a doctorate in neurobiology. Today, she is an associate professor in the department of cell biology and human anatomy at the school of medicine at the University of California, Davis. Her laboratory at Davis focuses on making retinal ganglion cells from stem cells with the goal of using these cells to replace damaged or lost nerve cells to restore vision. It is my honor to welcome Dr. Anna La Torre.
Anna La Torre, PhD: Thank you so much. Thank you for the introduction. It's my greatest pleasure to be here. Today I'm going to talk about the work we are doing together with the other members of the Catalyst for a Cure team. But before I show you our latest data, I would like to give you a very brief background on glaucoma, not as a clinician, but from my point of view, which is a cell biologist and a basic researcher.
So, as probably you all know, at the back of your eyes, there's a very thin tissue called the retina. This is the tissue that can capture and see light. In the lab, when we look at this tissue with special techniques under a microscope, we can see that the retina is made by different types of neurons. Some of these neurons are called photoreceptors, and these are the cells that can detect light. This information, this visual information, is then passed to other cell types in the retina.
These red cells here are called retinal ganglion cells. These cells have very long cable-like extensions. We call those cables axons that send this visual information from the retina to the brain. So here, every single one of these small dots is one retinal ganglion cell. This is an image from a retina if we look from the front. And as you can observe, all these cables, all these small filaments, are going towards the center of the retina, this region called the optic nerve head. In this region, all these little cables get together, bundle together, in a structure called the optic nerve. And the optic nerve is the only connection between the retina and the brain.
Unfortunately, glaucoma is affecting specifically and only these cells, the retinal ganglion cells, which is unfortunate, because by eliminating, by attacking these cells, we are cutting the only way of transmission of information from the retina to the brain. So what's really happening in glaucoma? You can see all these retinal ganglion cells send their fibers towards the center of the eye, toward this optic nerve head region. And in glaucoma, there's an insult, there's a problem in this eye. Often it is caused by elevated pressure, or intraocular pressure, in the eye. And when this happens, slowly these retinal ganglion cells get damaged. They get sick. Slowly these cables, these connections, start to break apart. And after that happens, the cells die, and they're gone. And this doesn't happen all at once. It happens progressively and slowly. And so, over time, we have less and less retinal ganglion cells. And unfortunately this is ultimately the cause of vision loss in glaucoma, is when these cells have gone and the retina doesn't have indigenous mechanisms to replace the dead cells.
So how can we cure glaucoma? What can we do about this? Well, as in many other things in life, time is everything. So if we are able to diagnose glaucoma early on, then the best approach would be to try to preserve what you have and try to prevent your cells from getting sick, from breaking apart and dying. We call that neuroprotection.
If we catch the disease in sort of an intermediate state where the cells are still there but they're not healthy, the axons, these fibers are breaking apart, what we try to do is save them from death and try to regrow these axons. And we call that approach regeneration. But when the cells are gone, they're gone, and there's nothing to be preserved. So in that circumstance, the only options left, really, are to try to replace the cells with new cells. And we call that cell replacement.
Unfortunately, by the time many patients realize that there's a problem, many retinal ganglion cells are already lost. And that vision that's lost cannot be restored by either neuroprotection or regeneration. And so to really restore vision, what we need is the most challenging approach, really, which is cell replacement. In the Catalyst for a Cure team, we are not just trying one single approach. We're trying to advance technologies for neuroprotection, regeneration, and cell replacement. But today I'm going to tell you about the work we are doing in the lab in cell replacement. So yes, three different strategies.
Why do I say that cell replacement is so challenging? First of all, to replace the cells, we need to find a source of cells and inject them back into the eye. They need to stay alive and survive there. And then they need to grow axons. They need to regrow these cables. And the cables should not go anywhere, they should go towards the center of the eye, towards the optic nerve, and then grow all the way towards the right visual centers in the brain and establish connections with the parts of the brain. So these are not simple, not any of these steps is simple. And we're trying to tackle them one at a time.
So, the first one is: where we can get donor cells for these transplants. Probably a lot of people have heard about the concept of stem cells. What are stem cells, and what do we really have in the lab? Stem cells is a very general word. But when people talk about stem cells, they normally refer to something called pluripotent stem cells. What this means is a cell that's very, very similar to the cell from a very early embryo.
So you, me, and all the animals, really, started life as a single cell. The cell divides from one, to two cells, four cells, eight cells, 16, etc., until they form an organism. But at these very early stages of development when the embryo is really just a little ball of cells, each one of these cells has the potential to become a whole organism. Each cell can become heart, a liver, muscle, skin, and also eyes. So that potential, it's called pluripotency.
Obviously, we cannot use embryos all the time in the lab, especially human embryos. That has some ethical concerns. But luckily, in the year 2006, a Nobel Prize, Dr. Yamanaka discovered a way to transform any cell into pluripotent stem cells, to transform any cell into something that really looks like these early cells in the embryo.
So, these cells are called induced pluripotent stem cells, and we can make them in the lab from either a lab rat or we can make them from patients. And the only thing that it takes is a little skin biopsy. We can then grow skin cells in the lab, in a dish. We can expand these cultures, have lots of cells. And we learn how to reprogram them so they become pluripotent cells. These are called induced pluripotent cells. They weren't pluripotent before. We just made them in the lab.
And when we look at them, these induced pluripotent stem cells really look exactly like the embryonic stem cells of the embryo. And they have this potential to do anything in a body, including a retina, and including retinal ganglion cells. So, labs, not just mine, but lots of labs around the world, have learned how to use and culture pluripotent cells. We also have developed technologies to differentiate these stem cells, these pluripotent cells, into retinal neurons, including retinal ganglion cells.
So, for these, we use a technology called retinal organoids, which basically is culturing these stem cells as, really, mini retinas in a dish. We know how to do that by slowly changing the molecules, and the cues, and the media that we are feeding the cells, and they progressively and slowly become retinal neurons. They form these beautiful layered structures that are very similar to the real retina with the different layers of neurons that we see.
And not only do they make the cells, the cells that we make, these retinal ganglion cells that we can derive in a dish from the stem cells, have many properties very similar to the real retina. For example, they extend these very long cable-like extensions, axons, similar to the real deal, the real cells in a retina.
These retinal organoids are really small, and the reason why they have to be that small, is because they don't have blood supply. And without blood supply, an organ can only grow so much. But an advantage is that we can make as many as we want, because the stem cells can divide, and divide, and replicate themselves many times. So now we have the potential to reprogram skin cells into IPS and to make retinal cells from them.
Not only that, we can also engineer the cells that we make to make them better. And what I mean by better, I mean that we can modify or manipulate some of their genes to try to get them to survive better, to extend longer axons. Or, for example, in this case, what we did is we got them to express a red color, a red protein, only the cells that would make a retina.
Why would we do that? It's not just because they're pretty. They are, but it's because that allows us to really monitor how many retinal cells we're making in the dish, are they dying, when are they being born, and how many we are making. So these kind of tricks allow us to really be able to follow what we are doing in these dishes. And this is just a picture to show you how small they really are.
And so with these technologies, now we can see the cells very well. And this is an example of one of these organoids. And we can see that about half of these organoids, the red part, is a retina. It's a laminated retina that develops all these cells, including these cells in green and blue, which are the retinal ganglion cells. But part of this organoid is not. So having these colors is also allowing us to sort the right cells from cells that we wouldn't want transplanted in an eye, for example.
So, with these organoids in a dish, we can do many things. We can screen for drugs that promote survival or, for example, axonal growth, to grow these little fibers. We can also really study in a very easy system why the cells get sick under different conditions. But our real goal is to obtain lots of donor cells for transplantation.
So it seems like we are ready for that, but there are still some challenges that we need to overcome. One is that the production of retinal ganglion cells in these cultures, this is still insufficient. We can make them. They look good. But as you can see here, the retinal ganglion cells are the green ones. We still have way more red cells than green cells. So we would like to increase the production so we can translate this to a clinic in an efficient way.
But the biggest problem is that, over time, the cells that we create in a dish die. And so, together in collaboration with the other Catalyst for a Cure team members, we're trying to find ways to help the cells survive better, not only in a dish, but also after we can transplant them. And so Dr. Derek Welsbie has been studying molecules and drugs that promote protection, neuroprotection, so they promote the survival of these cells for many years. And he's found some very interesting candidates.
This is a normal eye, and this is how many retinal ganglion cells are there. This is an eye where it got injured, and these ganglion cells are dying and disappearing. And this is an eye that got injured, but had one of these neuroprotective agents. And you can see that these drugs allow many, many more cells to survive this damage. So we are trying to see if the same drugs, the same neuroprotective agents, work for the cells that we make from the stem cells. And the answer is yes.
We found several drugs that can promote survival of the retinal ganglion cells that we can create from stem cell cultures. And not only that, not only have we found drugs that promote survival, we also found some drugs that promote both survival and axonal growth. So, compared from the controls where the cells look like neat little neurons with a body and a small cable, you see that when we treat these cultures, now the cells have much longer, healthier cables. And that's exactly what we want after we transplant these cells in an eye.
This is another example of a treatment that we found that promotes both cell survival and axonal growth in the cultures. And this is a trick that we do by culturing these retinal ganglion cells with another cell type of the eye called glia. And what we know is that when we mix these two cell types, or when we use the substances, the molecules that the glia produce, we can see that these ganglion cells survive better and have longer axons, which is very promising.
Another strategy that we are using to really increase production and survival of these cells before and after a transplant, together with Dr. Xin Duan and Yang Hu, is that Dr. Duan a long time ago discovered that some types of retinal ganglion cells ... I told you about retinal ganglion cells, but there's not a single type of retinal ganglion cells. There are several types. And they have different shapes, and express different molecules, and slightly different properties. So, what Dr. Duan found is that not all types of retinal ganglion cells are susceptible the same way to the glaucoma, to elevated pressure, or to damage. And while some cells just very quickly die, get damaged, get sick, and die, and they're gone ... We found some other subpopulations, other types of retinal ganglion cells that actually survive much, much better after damage.
And so what we've been trying to understand is why — why some types of ganglion cells can survive better when they're under this pressure and there's damage. And because now we understand some of the molecular cues that are promoting this resilience, we can engineer all the cells that we make from the stem cell cultures to become more like the resilient cells. So we can get them to survive better when there's a problem in the eye.
So, finally, what we are really trying to do, and this is very new and is really a work in progress, what we're trying to accomplish is to really be able to transplant the cells that we make in the dish into an eye, and to see if the cells can survive in the eye, extend axons, extend these fibers, and reconnect with the brain, because ultimately that would restore vision. And so we started doing these experiments. We can transplant cells in an eye. And the good news is that we see that some cells can survive after transplant for quite some time, for several weeks and probably months now.
We still don't know why some of these cells survive better than others after transplant, so we're trying to do these tricks to improve this process. And we don't know yet whether the cells can connect well. So this is all what we're trying to accomplish in the next few months, and what we'll be working very hard on in the coming months, to try to see if the cells after transplant can reconnect with the right parts of the brain.
I've been telling you about the power of stem cells, so I just want to add a little warning here. And it's that currently there are no FDA-approved stem cell treatments for glaucoma. The only FDA-approved treatment for glaucoma are drugs to lower the intraocular pressure. And those are the only safe, approved treatments, right now. There's lots of clinics that offer treatments for some money, and they try to exploit the most vulnerable patients. So please do not trust these places.
But I don't want to end with a sad or disappointing note. I don't want just you to take the message that we have a long, challenging way to go, because there's hope, and there's hope through research. And so if you think about it, we didn't know that we could make stem cells, reprogram cells, any cells, skin cells, to make induced pluripotent stem cells until 2006.
Now, it may seem a long time ago, but this was first discovered ever in 2006. By 2015, we already had the first clinical trial ongoing using IPS. Not for glaucoma, but for different diseases. And in the year 2020, we have 53 clinical trials ongoing using IPS. So research is moving forward. We are slowly but surely making progress. And I just want to thank everybody that's supporting the lab, and I would love to answer any questions that you may have. Thank you very much.
Tom Brunner: We're now ready for questions and answers. Thank you very much, Anna. That was so interesting. Our first question is, what do you think the timeline is? What do you foresee, how long before we'll reach clinical trials with these projects that you're working on?
Dr. Anna La Torre: That's a great question. I wish I had a very defined answer, and I don't. And the reason why I don't have a for sure answer is because research works in a kind of trial and error manner. We make lots of mistakes. We take avenues that don't go anywhere, and then we need to regroup and try something else. And there's never a clear path on, "This is the answer. This is the solution. This is what we need." We just try to overcome challenges as they come. My opinion, and this is my guess, is that we'll have a clinical trial probably in about 10 years from now. This is probably me being pessimistic, but there's a long way to go, and there's a lot of work that needs to be done to just make sure that we have the right cells, that the cells can connect to the right place. But mostly that, once we get there ... And I'm confident that we can have those sooner than that. Then there's lots of steps that need to happen to make sure that this is safe. Stem cells can divide. And because they can divide, they can have the potential to create a tumor. And we need to make sure that the cells that we inject have no stem cells, pluripotent stem cells, left. And that's going to take some time to make sure this is safe.
Tom Brunner: Well, it definitely is an exciting opportunity. And as you say, we have to be sure that it's safe and effective before we can really move into extended clinical trials. How optimistic are you that you may actually be able to restore vision for patients?
Dr. Anna La Torre: Very. Very [optimistic]. I have no doubts, the way science is advancing every single day. If you look back at where we were five years ago and where we are right now, the progress is incredible, and it's moving forward exponentially. So I have no question that we'll have tools to restore vision, not just for glaucoma, but for many other diseases in a few years. I'm also confident that, sooner, we'll have really good ways to protect cells. We'll have better diagnostics methods, so we're going to be able to catch glaucoma sooner than we are right now. Unfortunately, right now, by the time some people go to the doctor, a lot of ganglion cells are already gone, and that's that. And so you need to really use your drops and follow the instructions of your doctor to protect what's left. But I'm confident that with better diagnostics we'll be able to catch disease sooner.
Tom Brunner: And that's really the key, catching it sooner and working with your doctor. Preserving vision is much better than trying to replace lost cells.
Dr. Anna La Torre: Absolutely, yes.
Tom Brunner: Our next question is, will your research apply to all types of glaucoma?
Dr. Anna La Torre: Yes. At the end of the day, in all types of glaucoma, vision loss is caused by this loss of ganglion cells. And so replacing them will solve all types of glaucoma. Depending on the type of glaucoma, these kind of approaches, replacing cells, will have to go together with also controlling your intraocular pressure. If we put new cells, and they're also under this stressful environment and damaging environment, they will also suffer the damage. So both treatments will have to go together. But yes, this has the potential to really be useful for all types of glaucoma.
Tom Brunner: Who do you think will be the best candidates for retinal ganglion cell replacement?
Dr. Anna La Torre: I think the best candidates initially will be patients with big losses in visual field, people that really are at the advanced stages and where vision is damaged. I think these will be the best initial candidates because the other two approaches, both neuroprotection and regeneration, at those stages won't do that much. And so I think that will be the best candidates, at least initially.
Tom Brunner: And our next question, what are the sources of the stem cells? You mentioned using skin cells, but what would be the sources for the cells for glaucoma patients?
Dr. Anna La Torre: There are a few IPS lines, established lines, that labs share. You can buy them from technological companies. They are approved, and they're clean, and we can just use them. Obviously, these are not your cells, and so a transplant with something that's not really from yourself always has higher risks of rejection or triggering immune responses. So, to me, the ideal scenario would be that the source of stem cells are the patients themselves. We can make a very small biopsy, skin biopsy. It's about a two-centimeter skin cut. We can grow cells from each patient, reprogram them into making stem cells, and then differentiate them and make ganglion cells from them. Obviously, this approach is longer because it requires generating the stem cells initially. But at the end of the day, if we can really speed up and improve these technologies, making stem cells, the technology is really there already, the ideal source will be the cells from each patient.
Tom Brunner: Here's a very good question. One of the real challenges here is: how will you make sure that these retinal ganglion cells are programmed to make the right connections in the brain?
Dr. Anna La Torre: This is a very important question, because having the wrong connections is almost worse than [doing] nothing. We have the tools in the lab to really look at connectivity, which means looking at what the cell is connecting to. We have tools. Basically, we can add a little mark into these ganglion cells, and this mark can be passed to the next cell after they form a connection. And then we can look and ask, "How many cells, what part of the brain's got that mark," because they got the connection from these retinal ganglion cells. And so this is a way we can ensure that we have the right connections only. And when I started working on these problems, this was the one question that really worried me. We can make the cells, I'm positive. We can make stem cells. That's not such a big deal for us, right now. But how can we make sure that the cells connect right, and we don't get something that's bad? But after seeing how the cells behave in the lab, I'm very optimistic because what they do is that their cables, these axons that they make, like to grow together with other cables and with other axons. So if we can get the axons to go towards the center of the eye, even if there's big damage and lots of these cells are gone, there's always some part of the nerve that's left. If there's some nerve left, it means that the cells will grow with the nerve that's there. They will grow together with the indigenous cells from your eye. And then it's kind of a train rail, and they'll guide them to the right parts of the brain. And I've seen this behavior in the cells. The axons like to grow together, to bundle. And so that makes me very optimistic that this may actually not be as challenging as I thought it would be.
Tom Brunner: What about age? I think we know that glaucoma tends to affect people who are less young. And I just wonder, is that going to be a factor in treatment with these, say, young retinal ganglion cells, new retinal ganglion cells? Do you think it will be more, or less effective as patients are older?
Dr. Anna La Torre: This is very interesting. Right now, we think it may be better, it may be easier [with older patients]. And the reason is because the vitreous of your eye, the liquid that's inside of your eye, it's a very thick, kind of viscous substance. And as we age, it slowly breaks apart, and it becomes more liquid. What we think is happening is that these transplants, when we inject them in an eye and there's this very thick liquid, it kind of traps some of the cells. And some cells cannot make it to the retina, just because they're stuck in this very viscous vitreous. And as we age, because [the vitreous] is more liquid, actually it's a little easier. So that's one advantage of not being so young. But this is an important aspect to keep in mind. We don't know how the immune system will respond in the younger or older people. So these are all questions that we have in mind and that we need to look at. It's a good question.
Tom Brunner: Now, another question is about the types of ganglion cells that you're using, both to transplant, but also to the different hosts. I mean, are you transplanting both rodent and human-type ganglion cells? And at this point, I guess they're all models, all the transplants are in models of glaucoma, because there are no human transplants being done. But what's your thought in the survival of these different types of ganglion cells between the rodent models and actual human cells?
Dr. Anna La Torre: That's a good question. We obviously are not doing experiments on humans, so we are not injecting cells on human beings. But we do have in the lab stem cells, IPS, from mice and humans. And human cells are slower than mouse cells, but they behave pretty similarly, and they are just slower. It makes sense because development in mice from conception to an animal being born takes 19 days. That's it. By 19 days, you have a little mouse running around. And in humans, obviously, it takes nine months. We’re bigger, but our cells also do everything slower. But if you keep in mind the time scale, they're behaving pretty similarly. So they're going through very similar shapes and expression of molecules, in vitro. And mice and humans have different types of retinal ganglion cells, because the way we process vision in the brain. Mice are nocturnal animals; we are diurnal beings. But fundamentally they're behaving pretty similarly. So I don't think that survival for mouse and human will be different, and the same way that I don't believe that growing the axons, getting the axons to connect, would be different. Obviously, at some point, we need to move away or try bigger animals before we can do clinical trials. And we should try to really kind of trace the human cells very, very well, which we are doing with Dr. Duan. But I don't think fundamentally they're different.
Tom Brunner: But you are working with human stem cells now to see how they behave, that you can derive from skin cells and so forth? So you're learning a lot.
Dr. Anna La Torre: Absolutely. And we can compare, keeping the time scale in mind. So in mouse cells, it's three weeks. In humans, it's five months. But if we scale that time, they're pretty similar.
Tom Brunner: Another question was about possible supplements or vitamins that might be helpful. You mentioned about neuroprotection and restoration, and so this is one of the questions that often comes up. And I would encourage our viewers to also visit our website and ask that question, because there are quite a few papers and presentations on our website about supplements. And there are, in fact, some recommendations for healthy eyes, healthy body. But do you have any comments on that, Anna?
Dr. Anna La Torre: Yes, there are clinical trials ongoing to see the effects of vitamins in not restoring vision, but preserving vision in glaucoma patients. And I agree, healthy body, healthy mind, a healthy diet, that all helps. Not smoking, that all helps. And so if we get to the point where this is a reality, and we can do clinical trials, and we can really restore vision, these treatments need to be together with everything else to preserve the vision that you have left. And as I said, if we inject cells, those cells will also be suffering from everything that's going wrong in the eye. So one treatment cannot be by itself. It has to be in combination with everything else we are doing to lower intraocular pressure and preserve the cells that we have in the eye. So it's going to have to be in combination.
And that's one of the beauties of this Catalyst for a Cure approach, because Dr. Derek Welsbie has been studying neuroprotection his whole life. And I never thought about it, because I am not an ophthalmologist, and that's the end, and I study the beginning. And so by combining our expertise, now we are doing that, we are combining strategies to protect the cells from that in the stem cell cultures. And so this combination of expertise is hopefully what's going to move the technologies forward.
Tom Brunner: Actually, Anna, that's a good lead-in to another question here, which if you wouldn't mind sharing a little bit, I think it would be interesting to our participants: what was your motivation to become a scientist in the first place? And then what has the Catalyst for a Cure experience meant to you from a personal perspective, for your career and growth?
Dr. Anna La Torre: This has been amazing, for different reasons. My motivation for becoming a scientist was first that, I guess I'm curious, and I want to know how things work. And, to me, the ultimate machine that I love to know how it works is building a human. From one cell, that cell has all the instructions in it to build itself and to build a whole human. And if you have children, it's amazing that it works, that you have a child with 10 fingers and 10 toes, and a head, and it's beautiful, and it works. So that amazes me. And I guess the curiosity to understand how things work. And then, at some point, I wanted to work on something that would make a difference and that would help people. And there's so many people affected by vision loss. And at the beginning of my studies on glaucoma and vision, I didn't have any family members affected. And it's so common that now I do have relatives that now have glaucoma. So now the motivation is maybe even more personal. But I was very passionate about this before.
I've been doing science for a few years now. I started my PhD almost 20 years ago. Science can only move forward by collaborations. We cannot do anything in our little labs, in our little teams. It doesn't matter if you're a big lab. A big lab is 30 people. And we always stand on each other's shoulders to move forward. And it only works when we share. And the more open and the more we share, the more we can move forward. But that's not the way science works, in general, because we try to be collaborative and to learn from each other, but at the same time, we're competing for resources, we're competing for publications. And so it's a weird thing where if you want to move your science forward, and that requires learning from and sharing, but at the same time, there's this competition going on.
And so this approach of putting together a team [Catalyst for a Cure]... And it's a team not necessarily of people thinking the same way, but the opposite, people with very different expertise that look at the same problem in different ways, and getting them to work together in a way that's really a team. There's no competition here. We are all in it together. It makes such a big difference. We can be very honest with each other, and we can just work together. And so this has been wonderful. And I think this is how science should work for all ... NIH should learn from this, because that's the way to do science.
Tom Brunner: Well, thank you, Anna. And I think your answer there was very informative. And certainly Glaucoma Research Foundation has been a strong advocate of collaboration, and the Catalyst for a Cure is now almost in its 20th year. And believe it or not, we are influencing the National Institutes of Health, and the National Eye Institute, and there are many more collaborative efforts than there were when we started, 20 years ago. So progress is being made. I want to thank, again, Anna for making time for us and for such a wonderful presentation, and especially for your dedication to helping to restore lost vision.
At Glaucoma Research Foundation, we remain as committed as ever to helping glaucoma patients, especially during these very challenging times. The Glaucoma Research Foundation office has already been partially reopened, and our work has never stopped. We continue to advance our mission to cure glaucoma and restore vision through innovative research, and to provide information and education about glaucoma. Please take your vision and your health seriously. Visit your eye doctor and work with them to help you maintain your vision. Thank you again for your ongoing interest and support of Glaucoma Research Foundation.
Last reviewed on September 30, 2020