Professor Martin Collinson is based at The Institute of Medical Sciences in the University of Aberdeen, and has been working on the roles of the PAX6 gene in eye development and adult life for over 25 years.

He enjoys opportunities to make current research into aniridia and other eye conditions accessible to all those who are affected by or interested in the science of vision.

Martin is currently focused on understanding corneal health and the development of drugs that can prevent corneal opacity in aniridia, with the aim to develop eyedrops that prevent corneal disease.

He gave us an update on his work at our online conference on 27 July 2024. You can see Martin’s presentation in the video below, along with the transcript.

Transcript

[Tierney] So hopefully everyone’s had a little bit of a break, you’re feeling refreshed and ready for the second session of this conference, where we’re going to be started off by Professor Martin Collinson. He’s going to tell us about some of his great research he’s doing at the University of Aberdeen. So I’m going to hand over to you Martin.

[Martin] Hello everybody, thank you very much. Thank you very much obviously for asking me to present today.

What I’d like to be able to do for you is to describe some of the work that’s happening in my lab where we’re looking to develop therapies for aniridia-associated keratopathy.

This slide has a picture of the eye of somebody with aniridia and their experience and, if you can see, quite a severe corneal opacity.

And this is what we call aniridia-associated keratopathy, also called aniridic keratopathy or aniridia-related keratopathy, that’s all the same thing.

And as you’re probably aware this corneal opacity is a progressive condition that can happen in most people with aniridia to some extent as they get older.

The surface of the eye starts to vascularize, it gets blood vessels and can become inflamed and this can lead to loss of vision.

Not everybody will get the keratopathy as bad as this person here, but of course – and as we’ve heard earlier today – the lack of certainty about the extent to which keratopathy can affect people’s vision in the future is a very significant source of anxiety to both the people with aniridia and to their parents.

And what we’re trying to do in our lab is to be able to prevent this from happening, or in people where it has already happened potentially to reverse this opacity to maintain vision long into adult life.

Now for those of you who are familiar with aniridia keratopathy you may be aware that it’s treated as a so-called limbal stem cell deficiency.

This slide has a picture of two eyes. Top one is a healthy non-aniridic eye with a nice blue iris, and the lower eye is a vascularized inflamed essentially opaque cornea, due to a known limbal stem cell deficiency.

And to explain a bit of the background to this, the front surface of the eye, the cornea, is essentially a specialised skin, and just like for the rest of the skin cells fall off all the time, just through normal wear and tear due to abrasion, and they have to be replaced.

And our skin has stem cells that divide to replace the cells that are lost and so does the cornea. And you may be aware that the stem cells that maintain the cornea live around the edge.

The boundary between the blue bit on this side and the whites of the eyes has a population of stem cells that are dividing all the time, fairly slowly, to replace the cells that have been lost.

And in people where these limbal stem cells don’t work, either because of disease or injury – alkali burns for example – the surface of the cornea can’t be maintained, cells are falling off but they’re not being replaced properly, and you get the sort of opacity and vascularization that you see in the bottom eye here.

And this looks very much like aniridia-associated keratopathy. And historically the condition has been treated as a limbal stem cell deficiency and many people with aniridia end up getting limbal stem cell transplants from non-aniridic individuals.

And these can help with the maintenance and vision for a few months or even years, but they’re not a permanent solution.

In order to study aniridia we’ve been using in our lab a strain of mice that has PAX6 mutations like people with aniridia do.

Not everybody is totally comfortable with the idea of using these mice. But these are perfectly happy healthy mice. But just like people with PAX6 mutation they do have all sorts of changes to their eye.

So there’s two mice on this screen, the one on the left is a normal healthy mouse with big bright eyes, and the one on the right is a mouse with aniridia, it’s got a PAX6 mutation. You may notice its eyes are smaller, it’s the so-called small eye mouse.

We’re not bothered about the size of the eyes, what we do like about these mice is that they have aniridia, they have lens cataracts and they have a kind of progressive keratopathy.

The cornea, the front surface of the eye, goes cloudy over time as they get older and it really very faithfully recapitulates the human aniridia-associated keratopathy symptoms.

So I’ve had PhD students and other people using these PAX6 mutant mice. We’ve spent pretty much 20 years working out what the link is between PAX6 mutation and aniridia keratopathy.

And we’ve had students asking the questions, is this really a limbal stem cell deficiency? And as with most things in science the answer is maybe but maybe not.

And here’s a little cartoon of some experiments that a PhD student of mine did. There’s little cartoon mice. The mice in the top row are normal wild type mice and the mice in the bottom row are small eye mice with a PAX6 mutation.

And what one of my students did, we put the mice under a general anaesthetic and she gave them a little scratch to the surface of the eye.

The idea is that limbal stem cells are meant to respond to eye wounding by making more cells to replace those that are lost.

And in a normal wild type mouse that’s what happens if you scratch the surface of the eye.

Within 24 hours you’ll see this mouse has got one yellow eye, which we’ve used to represent activation of the limbal stem cells.

So we can see the limbal stem cells dividing at high rate in response to a corneal wounding, and after 48 hours the limbal stem cells in both eyes have activated. They’re really dividing as fast as they can to repair the injury.

We’ve already seen that PAX6 mutant mice do have limbal stem cells and they do divide and when my PhD student was able to wound the eyes of these mice, again just gave them just gave them a tiny little scratch to the cornea under anaesthetic, the limbal stem cells, they do wake up after 48 hours, they respond to the injury and they’re dividing to produce more corneal cells.

But the difference was that they took longer to do it. After 24 hours there was no response for the limbal stem cells. So there is a deficiency here. It’s pretty mild.

People and mice with aniridia do have limbal stem cells. Those stem cells can divide, but they take a little bit longer to respond to injury.

And the question is can that explain the whole problem with the cornea going opaque in aniridia? And we believe the answer is no.

This slide again just shows another person with aniridia-associated keratopathy, with blood vessels growing into the cornea and a big opacity in the cornea.

And the reason why this is happening is not because these people don’t have limbal stem cells. There’s much more going on.

There’s a whole lot of things going wrong in the corneal epithelium itself, and this is really what we spent 20 years trying to work out what the problem was.

And rather than give you a summary of 20 years of research, I’ll just describe briefly what the conclusions were.

And the problem essentially is that the PAX6 aniridic cornea, the surface is fragile. The cells don’t hold together as well as in normal non-PAX6 deficient corneas and what that means is that the cornea gets small lesions, small holes in it.

This is a figure that I lifted from an old paper and it’s not too important, but what four of the panels here are showing are scanning electron microscopy. So really clever imaging of the surface of the cornea.

And the first two, the top two panels, are really boring. It just looks like nothing really, because these are normal healthy wild-type corneas and they’re lovely and smooth and there’s nothing to see.

But the lower two panels C and D show corneas with holes in them, and these are from the aniridic mice. So cells are being lost too fast, because the cornea is fragile and it develops holes in it. And because of that it doesn’t really form an effective barrier to the outside world.

I don’t know if any of you at the ophthalmologists have had… they use fluorescein, a sort of fluorescent green dye, to determine whether the surface of the eye is healthy or not. Because a normal healthy cornea won’t take up fluorescein dye, whereas one where the epithelium is lesioned, it will.

And I don’t know if you can see down here, this is a section for a mouse cornea, all the cells are blue, and there’s a little stripe of green at the top where we’ve put fluorescein on the cornea, but it hasn’t penetrated.

Whereas this is a normal healthy mouse and this is a PAX6-deficient mouse and you can see that the yellow dye has spread throughout the whole cornea, that it’s no longer forming a barrier.

So this is essentially the problem with aniridic corneas. They don’t form a proper barrier to the outside world because they’re fragile.

So stuff gets in, and it’s not normally fluorescein, but it can be oxygen, noxious agents, dust, viruses, fungi, all sorts of things that are bad for the cornea that the cornea normally keeps out. but the aniridic cornea is just slightly less efficient at doing.

We came up with what we call our triple whammy model of aniridia pathology and it’s summarised in this diagram on the right here.

And at the top in blue is the start of the process, a PAX6 deficiency. So people with a mutation in one of their PAX6 genes, that means they don’t have as much PAX6 as normal.

And down at the bottom is the outcome corneal opacity. The cornea is no longer fully transparent and people start to lose vision.

And in between are the things that we think goes wrong. And it’s summarised on the left in the yellow writing with the so-called triple whammy model.

And whammy 1, as already explained, is the corneal epithelium in aniridia is fragile, and it loses its ability to act as a barrier to the outside world. So it’s under stress. Oxygen gets in, pathogens get in, and the cornea is under stress.

The second whammy, which I haven’t mentioned yet, is that normally when tissues are under stress, they produce protective enzymes that stop that stress from damaging the tissue.

And for a number of reasons aniridic corneas have lower levels of these stress responsive enzymes. So they are more stressed. They’re suffering more stress and they produce less of the enzymes that respond to that stress.

So that’s what these two yellow boxes are showing here. We have a fragile corneal epithelium with less of the protective enzymes that it needs, and this leads to increased stress. Proteins get oxidised that shouldn’t be oxidised, all sorts of cell sickling happens that shouldn’t be happening.

And this leads to a kind of chronic wounding state, even in the so-called healthy aniridic cornea. It’s constantly developing holes and then healing those holes, and then getting more holes and healing the holes again. It’s constantly in a wound healing kind of state.

And this leads to two things, one of which isn’t obvious, that it effectively reduces the amount of PAX6 that’s available.

Because PAX6, as you might know, is a gene, it’s a protein that controls the expression of a whole pile of other genes.

So it’s a DNA binding protein and DNA is in the centre of the cell in the nucleus But what stress does, and it’s one thing that we showed, is that it drives the PAX6 out of the nucleus.

So even the PAX6 that’s there in the cells can’t do its job properly, because it doesn’t get access to DNA.

So that’s what these arrows pointing backwards are showing. It exacerbates the PAX6 deficiency.

And because of the constant chronic wound healing state eventually the cornea becomes vascularized, blood vessels grow in that shouldn’t be there, it gets inflamed, water gets in, it disrupts the structure of the cornea, and over time you get a corneal opacity.

So this is 20 years of work that we have spent trying to work out why a deficiency of PAX6 leads to corneal opacity at all.

The question is, that’s very nice to know, but what do we actually do about it?

And our vision is that when a person has aniridia, we want to be able to give them therapies, eye drops or something similar, that will prevent this triple whammy model from taking effect, and will break the link between PAX6 deficiency and corneal opacity, such that good vision can be retained late into our adult life and at best for the rest of your lives.

And we’ve taken two strategies by which we’re attempting to do that. One of which, the left hand side here, is direct antioxidant therapy.

So if the problem with the cornea is oxidation and stress, then there are chemicals we could use to reduce that stress.

And the other kind of obvious strategy, the second one here in yellow, is the restoration of PAX6 activity, so as people with aniridia are deficient in the amount of PAX6 you produce, so can we restore that back up to normal levels?

And what the next slide is going to show is three streams of research that we have been undertaking to try and address these problems.

And number one on the left here is talking about two drugs that are in the public domain has been published as increasing PAX6 dosage in the eye.

One’s called duloxetine and one’s called ritensarin, and they’ve been shown in tissue culture, in the lab, in cultures of eye cells, that they can increase the amount of PAX6 that is produced by cells. And I’m going to describe some work that we’ve done putting these drugs into aniridic mice, to show what they can do.

The second stream in the middle here is something I’m not talking about too much about today. But those of you who’ve been involved with the aniridia therapy scene may have heard of a drug called ataluren, which is a type what we call a read-through drug which allows cells to ignore mutations in PAX6.

So even if you have one copy of the gene is mutated, within the presence of so-called read-through drugs the cells will ignore that mutation and produce normal PAX6 anyway.

And there is a drug called ataluren that has been one of these read-through drugs and it’s been trialled for aniridia. It didn’t really do a lot of good.

Nevertheless it’s not the only read-through drug out there and we are testing a whole pile of other read-through drugs to see if they can help people with aniridia.

And the third stream on the right here is the development of antioxidant therapies that will allow aniridia corneas to just get out of this vicious cycle of perpetual wound healing, to be able to sort of calm down and allow the regenerative capacity of the cornea to be restored, such that the loss of opacity doesn’t occur.

And what’s crucial about these three research streams is that we’re not coming up with new drugs.

What we’re doing is finding approved drugs that are already being used to treat people for other conditions. Like duloxetine for example, on the left here, is a known safe antidepressant.

And we’re saying we’re taking these drugs that already we know they’re safe to give to people, we know that they’ve passed clinical trials for other things, but we’re asking can they help people with aniridia?

And by taking this strategy, what we’re hoping to be able to do is to accelerate the process of identifying a drug that helps with aniridia, can be taken to through clinical trial and given to people, in the minimum amount of time.

Because as you’re aware with vision loss in aniridia, time is critical, and there are thousands of people out there that could benefit from a therapy, whose eyesight is frankly not getting any better. We want to minimise the amount of time that it takes to get drugs to helping people with aniridia.

So I’m just going to do a bit of science. I’m going to describe an experiment that we did last year actually, where we gave normal mice – so here’s our two friendly mice again, the one on the left is a normal wild type mouse and the other is one with a PAX6 deficiency.

And we gave them the drugs, these two drugs duloxetine and ritanserin, together in their drinking water for four weeks. And we monitored their eyes during the process, we also monitored the health of the mice to make sure that it wasn’t causing them any harm or side effects.

Like I said, duloxetine is an anti-depressant, ritanserin is an anti-psychotic, these are quite powerful brain drugs. But the dose was very low and we put these drugs in the mice’s drinking water.

And so did their eyes get better? And the long story short is that yes, they did.

On this slide here we have some mouse eyes. Mouse eyes have all the same bits as human eyes, but they’re not nearly as pretty really. And they have black irises and they’re much more like footballs.

Because whereas we are looking at things that are very far away, mice are basically looking at sunflower seeds that are very close to them, so they have a different shape eye. But otherwise their eyes are like ours.

And at the top of the screen here there’s two wild type mouse eyes, lovely and shiny, lovely and clear, a nice big black iris.

And bottom left here is one of the aniridic mice and it still has an eye obviously, but there’s severe loss of the iris, so iris hyperplasia or aniridia, and the surface looks a bit rough.

And they’ve had fluorescein treatments, so it’s yellow because this fluorescein has penetrated the eye in a way that it didn’t with the wild types. And you can see there’s a bit of a scar in the lens maybe.

And this is the heterozygous mice that didn’t get the drugs, these just got the controls and this is a normal aniridic mouse eye with lots of problems.

And this is an aniridic mouse eye that got the ritanserin and duloxetine combination therapy. And I hope you can see it’s better.

The iris doesn’t grow back, I mean that’s gone, there’s nothing we can do about that. But the surface of the eye looks nice and smooth, the barrier function has been restored so it doesn’t take up fluorescein very much either.

And essentially this mouse with the duloxetine ritanserin therapy has better vision than this mouse that didn’t have it.

Here’s some science of it.

One, these are tissue sections of the mouse’s corneas, and we’ve labelled the PAX6 protein fluorescent green so we can see it.

And top left is a wild type cornea, and you can see there’s a streak of green cells that has the normal levels of PAX6.

And this down here bottom left is a heterozygous, so PAX6 deficient cornea, and if nothing else you can see that there isn’t as much green in these cells as there is above, because these guys don’t have as much PAX6.

But going to bottom right, the heterozygous mouse after treatment, they have much more PAX6 in their corneas. So the drugs seem to be working, they’re increasing the amount of PAX6 that the cells can produce.

Another science bit, there’s two things on this graph, one of which is a tissue section through the cornea. And you may be able to see that in the epithelium here there are some bright pink blobby cells. They shouldn’t be there. These are conjunctival cells.

So one of the problems with aniridic corneas is that the epithelium with the whites of the eyes, the conjunctivum, starts to encroach onto the corneal surface, and it’s not transparent, and it’s vascularized, and that’s bad.

So what we want to do is to prevent this conjunctivalization from happening. And this is what this histogram on the right here is showing. Basically, the bigger the bar, the worse it is.

And we have control mice with no conjunctival cells, with or without drug. And this is an aniridic eye from the mice and they all have conjunctival cells. But after drug treatment it’s been reduced, so less than half of them now have conjunctival cells.

So within four weeks we’ve managed to push the conjunctivalization of the aniridic corneas backwards, just by giving the mice these drugs in their drinking water.

And that’s lovely and everything, but I’ve already said that these drugs are powerful. Duloxetine is a powerful antidepressant. ritanserin is a powerful anti-psychotic.

Our vision, as it is, is that when a baby or a young child is born with aniridia, we can start giving them drugs that will prevent the deterioration of vision. But we can’t be giving babies and young kids powerful antidepressants just for the ocular effect from the eyes.

What we want to be able to do is to develop eye drops, so that kids aren’t getting a systemic dose of these powerful drugs. They’re getting just a very small topical dose delivered right to where it’s needed to the eye.

We’re not as far on with these experiments, but we are doing a series of experiments where we give the mice eye drops.

So mice with aniridia, PAX6 deficient, twice a day, putting a little blob of gel in their eyes that contains either nothing – the controls – or that contains duloxetine and or ritanserin. And this is an experiment where we did it for two weeks.

Again, aniridic mouse eye on the left looking a bit rough. This is a control. Aniridic mouse eye on the right that’s had duloxetine ritanserin eye drops for two weeks.

And I have to say it doesn’t look like there’s a massive difference. It hasn’t been as effective as the drinking water was.

But we do all sorts of analyses on these things and we showed that it’s not doing any harm, that cell division is normal, that the gross health of the eye seems to be improved a bit, but not massively. And we can look at gene expression in these things.

And this is the last science slide here. And it’s kind of backwards. We’re looking at the thing on the right first. In this graph here, the higher the bar, the better.

We’re looking at an expression of one of the proteins that holds the cornea together. It’s called cytokeratin, it’s one of the proteins that stops the cornea from falling apart.

And normally in people with aniridia the cornea doesn’t produce as much of this protein, it’s one of the reasons why it’s fragile.

And this is a healthy mouse eye and it’s producing loads of the stuff, a big bar.

And the control aniridic eye still produces some keratin-12 but not as much as it should. But after eye drop therapy it goes right up back to normal.

So using these eye drops, we’re restoring normal levels of expression of one of these key proteins that stops the corneal surface from breaking up.

The left hand side of this science slide is something that I haven’t really talked about yet, but these are using antioxidants.

So giving the aniridic mice have antioxidants in their eye drops, does it reduce the stress? Does it put out the fires that the aniridic cornea is normally fighting? And the answer is to some extent yes.

So in this graph, the lower the better. And because this is an aniridic cornea with lots and lots of stress… a wild-type, a normal cornea, would have virtually none, it would be down at the bottom somewhere.

And an aniridic eye that we’ve given antioxidant drugs to, the stress is reduced and the cornea is calming down, and we’re hoping that will give it time to heal.

So this is where we are at the moment. We still have quite a lot of work to do. But I’m gonna stop and I’m gonna summarise essentially where we are.

So on this slide we have our conclusions.

And on the left is a piece of artwork we did which describes the process of working on aniridia. And it’s some sort of science-based Sisyphus pushing a giant transgenic eyeball up a big hill, and every time he thinks he’s made some progress he wakes up next morning and finds that the eyeball is back down at the bottom of the hill. And he’s in a landscape of inflamed eyes.

But the essence of what I’ve been talking about is that we are trying to develop eye drop therapy that can be given to people with aniridia to either prevent the corneal opacity from ever happening, or in people where it’s already happened to stop it or to reverse it.

And in order to do that, we are testing, we are using drugs that are already approved for something else and asking the question can they increase PAX6 dosage? Can they improve the health of the of the aniridic eyes?

And we’ve shown that two of the candidate drugs that are already in the public domain, duloxetine and ritanserin, are really quite effective at improving corneal phenotype, the eyes of mice.

And we are testing new versions of the drug ataluren. So again many of you will remember there was a drug called ataluren which has been used in clinical trials for aniridia. It hasn’t really been very effective and we’re looking at a whole panel of things that might be better versions of ataluren.

We’re actually quite excited to find that antioxidants can be quite effective at reducing the stress within the aniridic corneas, because these are very widely available and they’re not even drugs. You can very easily dose up on antioxidants and it may well improve the phenotype, the symptoms of the cornea over time.

And so there’s lots of things to be optimistic about. But as always with these things there are lots of caveats, lots of questions and lots of work still to do before we’re at a stage where we’re seriously proposing putting these drugs in aniridic eyes.

I have to thank some people. So on this slide, this sort of great pancake here, is an aerial view of Aberdeen. It’s not the most inspiring looking place in the world, although it’s nice and sunny today I have to say.

We’ve been funded by Medical Research Scotland and the NHS Grampian Endowment Research Fund to do this work, so we are making some clinical backing for this work, although as always we’re short of cash.

And quite a lot of the work that’s described today wasn’t done by me, because I just sit around drinking tea. It’s done by the postdoctoral person here. This is my lab. I tried to take a photo, but it went as well as you might expect.

But most of the work has been done by this person here, Kaya Kostanjevec, with Yakup Yilderim, Tereza Senfeld, Solène Moreira (who’s not on this slide), Anouk Cohen-Solal and Yvonne Brown. And of course we’re all based at the University of Aberdeen.

So I’m going to shut up. If you have any questions about the work, I’ll be very, very happy to take them.

[Tierney] Thank you very much Martin, that was really, really interesting work.

So we do have some questions in the chat and the first one is can you give some insight into the efficacy of the existing eye drops that many aniridics already take?

[Martin] I’m not an expert in this, but I mean eye drops that people with aniridia take will be primarily aimed at protecting the surface of the cornea.

So prevention of dry eye is really important, making sure that the corneal surface is moist.

Obviously people may be taking anti-glaucoma drugs as eye drops and that’s very effective, there’s no problem there.

But there really remains no treatment that prevents the underlying causes of why aniridia-associated keratopathy happens in the first place.

So generally looking after the eyes is obviously a good thing. But there’s no therapy currently that for example increases the PAX6 dosage in the corneas. Everything is aimed at the symptoms and there’s nothing really associated with the causes.

[Tierney] Yeah, I think there’s quite a lot of issues at the moment, in terms of having that preventative treatment over dealing with the issue once it’s already there.

We’ve got a question with regards to what are the levels of the dosage regarding the drugs that you’re using, compared to the dosage they normally are related to for their antidepressant and antipsychotic roles?

[Martin] The good news is that it’s much smaller. They are much more effective at increasing PAX6 dosage than the dosage that they are given as antidepressants.

If you scale down the human dosage to what a depressed mouse might for example get, then the dosage we’ve been given to improve the eye phenotype is about a quarter of that.

That still does have a subclinical effect though. And although it’s probably safe to give kids duloxetine at a very low dose, one of the real reasons which we’re developing eye drops is to avoid that systemic dose.

If you give people the drugs as eye drops it goes straight to the target and the systemic dose that they get across the whole body will be essentially undetectable.

So the summary is that it’s a very low dose, but even so we’re trying to minimise it as much as possible, such that there’s little risk of non-target effects.

Because clearly if we develop some eye drops then the idea is that people will be taking them for their entire life, so we have to be really careful that there’s no side effects.

[Tierney] Yeah that makes sense, thank you so much.

So next question, they said you’ve done some amazing work over the last 20 years to get to this point. How long would you guess before it would be potentially available to patients? How much more work is involved?

[Martin] That’s always the million dollar question isn’t it? So we work closely with some patients and they ask the same thing.

I wouldn’t be doing it if I didn’t think we could get something within the next two or three years. That’s the target, maybe even less.

I mean, I’ve got a PhD student starting in October whose job is to start to try to take these things to clinical trial. So we’re optimistic that we can do things quickly.

But, you know, I’m very old now, I’ve had lots of disappointments in my life, and I don’t want to give people false hope that there’s something just around the corner. Unexpected things may crop up and there may be a delay.

But so far the signs are very good and we’re very hopeful that we can get something going within a couple of years.

[Tierney] Brilliant, I’m sure we all have our fingers crossed that your work goes smoothly. But yes, there’s always trials and tribulations to work through.

One of the last questions we’ve got here is do you hope that this approach might be able to actually reverse current keratopathy damage that’s already occurred in the future?

[Martin] We’re really hopeful that it can.

One of the things that not just us but lots of scientists have shown in the last 20 years is the cornea has tremendous powers of regeneration, and that if you give it a chance it will repair.

And the problem at the moment for people with aniridia is as the opacity develops the cornea is being overwhelmed beyond its regenerative capacity.

If we can increase that, give it a chance to regenerate by reducing the stress or increasing its PAX6 dosage, there’s every reason to hope that existing damage can be reversed, that we can make the blood vessels go back and give the corneal structure time to repair. I don’t see any reason why that can’t happen.

As with all human conditions, I think it’s going to be better to catch it early and stop it from happening, than to try and reverse it once damage is done.

But I’m very optimistic. I believe the power of eyes to regenerate has been shown lots and lots of times, that the cornea is a tremendously adaptable and strong tissue. And I see no reason why we can’t restore vision in people that have already started to lose it.

[Tierney] Brilliant, thank you so much Martin, I’m sure we’re all very intrigued and can’t wait to see what happens to your research over the next few years.

I think we’ve got one final question here that’s just popped up. So in regards to antioxidants, are we referring to over the counter and contributing of good diet?

[Martin] Yeah, I’m very tempted to say that eating a good diet can’t be a bad thing, because a good diet is never a bad thing I guess.

What we’ve been looking at is there are some over the counter antioxidants, eye drops, that people get for various inflammatory conditions. And we’ve been not using them, but we’ve been using some of the components of them.

So the reason we’re not using over the counter medications is that they’ve been reported to be quite irritating for the eye, that they sting a bit when they go in, and to try and persuade kids to do that. But also because the aniridic cornea is fragile, we don’t want to cause anything that’s going to be an extra irritant to it.

So we’re looking at over the counter antioxidants, but we’re trying to see what we can do with them that makes them safe for aniridic eyes. Because at the moment I’m not totally sure they’re a fantastic idea for people with aniridia.

[Tierney] Brilliant, thank you so much Martin.

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Thank you to Glen for the video editing and write-up.