Fitness

Rejuvenating the retina to save vision

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4 months ago

May 29, 2024

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A series of four eye irises are arranged in a line against a black background.

Frederick Miller how environmental and genetic factors contribute to autoimmune diseases.

We’ll chat about these topics

What are the subtypes and causes of myositis, a rare pediatric autoimmune disease?
How do genes and the environment contribute to autoimmune diseases?
Why are autoimmune diseases becoming more common?

Friday, June 28th, 2024 | 11:00 AM – 11:45 AM Eastern Time
This listen in webinar will be available to view live and on demand.

Do you have your own questions about the science of autoimmunity? Bring them to the Listen in event and let’s discuss!

Featured researcher

Fredrick Miller, MD, PhD

Scientist Emeritus
National Institute of Environmental Health Sciences

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The human brain, with its incredible complexity, is one of the most challenging organs to study. Traditional animal models often fail to capture the intricacies of how the human brain develops and functions and how brain disorders come about. In recent years, there have been exciting advancements in creating advanced 3D brain models that more closely mimic the brain’s structural organization and environment in vitro. In this webinar, Madeline Lancaster will discuss how her team creates cerebral organoids and uses these in vitro models to better understand human brain development and neurodevelopmental diseases.

Topics to be covered

Creating self-organizing cerebral organoids from human pluripotent stem cells
Using cerebral organoids to investigate human neurodevelopment and neurodevelopmental disorders

Thursday, June 20th, 2024 | 11:00 AM – 12:00 PM Eastern Time
This webinar will be available to view live and on demand.

Speaker

$\"Madeline$

Madeline Lancaster, PhD

Group Leader
Medical Research Council Laboratory of Molecular Biology

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Topics to be covered

Creating self-organizing cerebral organoids from human pluripotent stem cells
Using cerebral organoids to investigate human neurodevelopment and neurodevelopmental disorders

Thursday, June 20th, 2024 | 11:00 AM – 12:00 PM Eastern Time
This webinar will be available to view live and on demand.

Speaker

Madeline Lancaster, PhD

Group Leader
Medical Research Council Laboratory of Molecular Biology

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age does the immune system weaken? “,”summary”:”After decades of combating daily assaults, the immune system undergoes dramatic changes that drastically affect human health. “,”slug”:”explained-at-what-age-does-the-immune-system-weaken”,”contentType”:”Explainer”,”displayType”:”Conversion”,”prominentUntilDate”:”2024-05-09 13:46:32″,”publishedDate”:”2024-05-09 13:46:32″,”body”:”

As hair grays and lines creep into the corners of a once youthful face, the immune system also ages. This internal biological aging triggers a cascade of molecular events, from reduced T cell production to increasing levels of inflammation, that leave individuals susceptible to infectious diseases and illnesses.

Download this Explainer Article from Drug Discovery News to learn about biological aging and how the immune system changes with the passage of time.

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Download this Explainer Article from Drug Discovery News to learn about biological aging and how the immune system changes with the passage of time.

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In diabetic macular edema, senescent cells build up in the retina, leading to vision loss. A new drug forces these undead cells to die, healing the retina.

Current treatments for diabetic macular edema, a severe form of diabetic retinopathy, are effective in most people, but not everyone. Now, building off of almost a decade of research, scientists developed a new way to treat diabetic vision loss by targeting senescent cells in the retina.

Host: Stephanie DeMarco, PhD, Associate Editor, Team Lead

Guests:

Mike Sapieha, University of Montreal and UNITY Biotechnology

Dorota Skowronska-Krawczyk, University of California, Irvine

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Transcript

Stephanie DeMarco: Hi everyone! Welcome back to another episode of DDN Dialogues. I’m your host, Stephanie DeMarco.

In today’s episode, we’re talking about something a little on the spooky side. No, this did not suddenly become a horror podcast; it’s still the DDN Dialogues that you know and love. But today’s story is about the undead — undead cells, that is.

These cells aren’t technically dead, but they aren’t really alive either. Instead, they exist in a sort of purgatory called senescence.

Sometimes, when cells find themselves in a stressful situation such as experiencing DNA damage, telomere shortening, or low oxygen environments, they can stop dividing. But rather than entering normal cell death pathways, these cells simply hang around.

Mike Sapieha: And so, these cells, they start to produce different inflammatory factors.

DeMarco: That’s Mike Sapieha, an eye disease and cellular senescence researcher at the University of Montreal as well as the chief scientist at the company, UNITY Biotechnology.

Sapieha: Initially, we think these factors are there to help repair the tissue, so there’s some regenerative factors and so on. And eventually, these factors switch to something that’s more, really purely proinflammatory, and we think this is to call in the immune system so the immune system can clear these cells out. And really, the problem is once the immune system is no longer able to clear the senescent cells, and they just reside in a tissue where they remain metabolically active but are no longer really able to contribute to tissue function.

DeMarco: This collection of inflammatory molecules, growth factors, and proteases that senescent cells release is called the senescent associated secretory phenotype or SASP. If immune cells can’t get rid of senescent cells fast enough, SASP can actually cause nearby cells to become senescent as well — just like a zombie spreading its zombifying-infection.

Research in mouse models has shown that senescent cells contribute to aging and age-related diseases including a decreased lifespan, cataracts, and premature infertility. A little less than a decade ago, scientists discovered that senescent cells accumulate in the eye in certain ocular diseases such as glaucoma and diabetic retinopathy. Over the years, Sapieha and others have shown in animal models that when they decrease the numbers of senescent cells in the eye using drugs that specifically target them, which are called senolytic drugs, vision and eye health improve.

Now in a recent study, Sapieha and his colleagues took their research one step further. They developed a senolytic drug that they deliver directly to the eye, and they tested this new drug class in people with diabetic macular edema for the very first time. They found that not only was the drug safe but that its beneficial effects may last longer than the currently available treatments, providing a much-needed new way to treat diabetic macular edema.

If you were to look so deep into the eye that you could see the retina, you might be surprised just how many blood vessels support it. The retina is responsible for vision, which takes a lot of energy. This means that it needs a lot of power in the form of oxygen and metabolites from the blood. This abundance of blood vessels also means that the retina is very sensitive to any metabolic disturbance or stress from the bloodstream. One of the most common stresses is high blood sugar due to diabetes. This hyperglycemia in the blood can first lead to diabetic retinopathy, and if it progresses, then to diabetic macular edema.

Sapieha: There’s around 93 million people worldwide that are affected with diabetic retinopathy. Of them, a subset will develop diabetic macular edema, and it’s really characterized by leaky blood vessels.

DeMarco: In the retina, endothelial cells form a tube around a blood vessel. Just on top of them sit cells called pericytes, which support the endothelial cells.

Sapieha: These endothelial cells and pericytes start to lose their ability to form junctions properly, or there’s some proteins that are secreted in the diabetic retina that cause these endothelial cells and pericytes to lose junctional integrity. And so, essentially, there’s contents of the blood that extravasate into the retina. So eventually, what happens is that you have a swelling of the retina. And, you know, in some of the worst cases, you can have little ruptures of blood vessels or little aneurysms, and then you can actually have blood in the vitreous. So that’s kind of like a spectrum of this diabetic macular edema, and it really is one of the main causes of loss of sight in the working age population, so a big cause for public health concern.

DeMarco: Currently, doctors treat diabetic macular edema with anti-vascular endothelial growth factor therapies also known as anti-VEGF therapies. These drugs tend to work well in many patients, but not in all of them. The other downside is that these drugs have to be delivered via an injection into the vitreous of the eye every six to 12 weeks, and their effectiveness can weaken over time.

So, when Sapieha and his colleagues noticed a surprising abundance of senescent cells in the retinas of people with diabetic macular edema, they wondered if there was another way to treat this condition.

Sapieha: And we had put out this initial study in 2016, showing that in models of diabetic retinopathy or mouse models of retinopathy of prematurity, there was a big accumulation of senescent cells, and that these cells were actually quite central to causing some of the vascular abnormalities that you would see in this disease.

We think that endothelial cells, when they become senescent, they fail to form proper junctions with their neighboring cells. And they also give up this SASP, this inflammatory secretome. So, we tried to initially just block the secretome. We got some pretty interesting data there. But from a therapeutic perspective, we thought it might be a better idea just to go and eliminate those senescent cells with a general approach called senolysis, so trying to find susceptibility nodes in senescent cells that can be targeted to send the senescent cell into an apoptotic cell death.

DeMarco: So, that’s exactly what Sapieha and his team did in their new study. First, they showed that a long duration of high blood glucose levels led to DNA damage and cellular senescence in human retinal vascular endothelial cells. Then, they asked, what would happen if they treated diabetic rodent models with a drug that targets senescent cells for destruction.

Sapieha: By eliminating those senescent cells, we were getting much more vascular integrity. So, the blood vessels were actually holding their content much more effectively in models of diabetes, and this led to increase in retinal function. So, we can measure the neuronal transmission in a mouse’s eye, and we found that this was improved with our senolytic treatment in diabetic mice. And so, this led to a clinical trial where we tried a senolytic approach.

DeMarco: Sapieha and his colleagues at UNITY Biotechnology developed a small molecule drug called UBX1325. This molecule acts as a prodrug. When the researchers inject it into the aqueous environment found in the vitreous of the eye, it dissolves easily and releases the active senolytic drug called UBX0601. UBX0601 then inhibits a protein called BCL-xL, which sequesters cell death proteins. Without BCL-xL, senescent cells undergo apoptosis and die.

Sapieha: Cells that are not senescent have different backup mechanisms for survival. So, they don’t only rely on BCL-xL. And cells that were senescent were really the cells that would disappear after treatment via this mechanism.

DeMarco: The researchers then recruited eight people with advanced diabetic macular edema who no longer responded to anti-VEGF therapy in their Phase 1 clinical trial. They found that patients tolerated the drug well, and when the team looked at the preliminary effectiveness of the drug, they were very excited.

Sapieha: With one single injection, patients had meaningful gains in vision that lasted six months. So to put that in perspective, so typically, with the anti-VEGF therapies, you would get an injection every six weeks. Now it’s the newer formulations, you could go up to three months or so. So, this was really kind of the longest period with a single injection that that was noted, so we were quite happy with that outcome.

DeMarco: University of California, Irvine vision researcher, Dorota Skowronska-Krawczyk also studies how aging and senescent cells affect the eye. She was not involved in this new study but was impressed by the research.

Dorota Skowronska-Krawczyk: One of the things that strikes very much is the very nice step by step work in the animal model, and then move to the clinical trial. And then the clinical trial shows amazing data. So together with the happiness for the concept working actually in human disease, there is also this component that there’s potential new therapeutics. Having said that, there is a very interesting point that everybody is thinking about is, how come only one injection can work so well, and for so long?

Sapieha: We think that what happens with the senolytic approach is that you’re really disease modifying, so you’re changing the nature of the damaged tissue, eliminating a lot of the damaged cells, and then allowing the healthy cells that remain to regenerate and to repopulate those areas where senescent cells once lived. So, all in all leading to these really long-term beneficial effects.

This is a drug that’s really driven by the pharmacodynamics, not the pharmacokinetics, meaning the drug is essentially out of the eye within five days or so. And so, it’s half-life is just a bit over a day, and essentially, what it means is that the drug is going in, eliminating the senescent cells, leaving the eye, and then the retina remodels itself or repairs itself. So, it’s really in contrast to, for example, an antibody or a corticosteroid, where you really want it to stay in the tissue for as long as possible to exert its action. So, we really do come in, repair the retina, and leave is the way that we believe this works.

DeMarco: Sapieha and his team are currently recruiting more people with diabetic macular edema for a Phase 2b trial so that they can better evaluate the effectiveness of their senolytic drug.

Sapieha: So we’re going head-to-head with anti-VEGF, and we’re very much looking forward to seeing the outcome of that trial. And we’re enrolling our patients at a good pace, so we should have our data in the beginning of 2025.

The next obvious steps are to see what other diseases that are characterized by a heavy senescence burden can benefit from senolytic therapies. So, that’s certainly what we’re thinking about moving forward. Whether they’re diseases of aging or chronic diseases, how they can benefit from senolytic therapies.

DeMarco: Most of all, having a new therapeutic strategy for diabetic macular edema and other conditions with a buildup of senescent cells is exciting for the field overall.

Skowronska-Krawczyk: The concept is pretty simple: to remove senescent cells and to improve health of the retina. The concept works, so it’s beautiful. I can say probably for many researchers, it was like really great data and then some kind of a huge hope — I am not exaggerating — for many age-related eye diseases.

Sapieha: Most exiting here is it’s really a new class of drugs, so it’s a new approach. There’s been a lot of really talented people working on the concept of cellular senescence, so building the whole biology up, and then for us to really be able to test these hypothesis in a clinical trial, and really provide some of the first evidence that a senolytic drug can exert the biology that we believe and that others believe it can was extremely rewarding, so I think that was probably the most exciting part of this whole project for sure.

DeMarco: That’s all we have for this episode of DDN Dialogues. I’d like to thank Mike Sapieha and Dorota Skowronska-Krawczyk for talking with me, and thanks to all of you for listening! Until next time, I’m your host Stephanie DeMarco.

This episode of DDN Dialogues was reported, written, and produced by me. To never miss an episode, subscribe to DDN Dialogues wherever you get your podcasts. And if you like the show, please rate us five stars and leave a review on your favorite podcasting platform. If you’d like to get in touch, you can send me an email at sdemarco@drugdiscoverynews.com.

And, the next time you watch a zombie movie, remember the power of senolytic drugs to get rid of damaging, undead cells and allow the eyes to heal.