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A Turning Point in Retinal Neovascular Diseases

Retina World Congress 2025 will take place May 8-11. As researchers prepare for their, presentation, we are highlighting the upcoming sessions that are scheduled for this meeting, which will be held in Fort Lauderdale, Florida.

Note: The following list of presentations are in alphabetical order by company. Updates will be added to this article as new information becomes available.

The company highlight Phase 2 results for migaldendranib (MGB), Ashvattha’s investigational subcutaneous treatment for wet age-related macular degeneration (wet AMD) and diabetic macular edema (DME). The presentation, entitled, "Emerging Data om Anti-angiogenic Nanomedicine (Migaldendranib MGB/D-4517.2) for AMD and DME" will be given by Michael Singer, MD on Sunday, May 11, 2025; 11:11 – 11:16 am ET.

Phase 2 clinical data demonstrated that MGB administration lowered production of subretinal fluid reducing or eliminating the need for intravitreal anti-VEGF treatment in both the study eye and fellow eye in wet AMD and DME subjects with bilateral disease. New data indicates that MGB may be the first safe systemic therapy for the treatment of wet AMD and DME without ocular adverse events.

Huma Qamar, Chief Medical Officer at Ocugen will represent Ocugen at Retina World Congress to share a presentation and join retinal surgeons and industry peers during a panel discussion.

Inherited and Rare Retinal Diseases Session
Moderated by Rishi P. Singh, MD, FASRS and Kourous A. Rezaei, MD on Thursday, May 8, 2025, 10:35 – 11:12 AM ET

Ocular Therapeutix will present information at the meeting in Fort Lauderdale regarding the axitinib intravitreal hydrogel clinical trials, the use of its candidate OTX-TKI for diabetic retinopathy, and the HELIOS clinical trial for diabetic retinopathy.

Axitinib Intravitreal Hydrogel: Update on Clinical Trials

Presented by Carl C. Awh, MD, FASRS, on Friday, May 9, 2025, 4:33 – 4:38 PM ET.

Presented by Dilsher S. Dhoot, MD, FASRS on Saturday, May 10, 2025, 8:44 – 8:49 AM ET

Volumetric Macular Fluid Analysis of the Impact of a Single Axitinib Intravitreal Injection (OTX-TKI) from the HELIOS Clinical Trial for Diabetic Retinopathy

Presented by Carl J. Danzig, MD on Saturday, May 10, 2025, 8:52 – 8:57 AM ET

The company will present further insights from Stage 1 of the Phase 3 DIAMOND program reinforcing the efficacy and safety profile of OCS-01 eye drops for DME will also be shared. OCS-01 is being developed to be the first non-invasive treatment for DME, addressing key unmet needs for earlier treatment intervention and for inadequate responders to the current standard of care.

Ashvattha Therapeutics to Present at ARVO, Retina World Congress, and AOS Annual Meeting. Ashvattha Therapeutics. April 15, 2025. Accessed April 16, 2025. https://www.globenewswire.com/news-release/2025/04/15/3061682/0/en/Ashvattha-Therapeutics-to-Present-at-ARVO-Retina-World-Congress-and-AOS-Annual-Meeting.html

Ocugen to Present on Modifier Gene Therapy Platform at Association for Research in Vision and Ophthalmology 2025 Annual Meeting and Retina World Congress. Ocugen Inc. April 29, 2025. Accessed April 30, 2025. https://www.globenewswire.com/news-release/2025/04/29/3070074/0/en/Ocugen-to-Present-on-Modifier-Gene-Therapy-Platform-at-Association-for-Research-in-Vision-and-Ophthalmology-2025-Annual-Meeting-and-Retina-World-Congress.html

Ocular Therapeutix™ to Participate in Upcoming Investor and Scientific Conferences. Ocular Therapeutix. April 29, 2025. Accessed April 29, 2025. https://www.globenewswire.com/news-release/2025/04/29/3070022/0/en/Ocular-Therapeutix-to-Participate-in-Upcoming-Investor-and-Scientific-Conferences.html

Oculis to Present its Innovative Late-Stage Pipeline Candidates at Upcoming Ophthalmology Conferences. Oculis Holding AG. May 1, 2025. Accessed May 1, 2025. https://www.biospace.com/press-releases/oculis-to-present-its-innovative-late-stage-pipeline-candidates-at-upcoming-ophthalmology-conferences

Companies working in the retina space have announced that data from clinical trials will be shared at this year’s meeting in Fort Lauderdale, Florida.

RWC 2025: Companies to share data at meeting in Fort Lauderdale

Amir H. Kashani, MD, PhD, is a professor of ophthalmology at the Wilmer Eye Institute in Johns Hopkins University in Baltimore, Maryland. In an interview with 

, Kashani discussed a research paper on OCT-A angiography's potential in detecting early signs of neurodegenerative diseases like Alzheimer disease. 

The study aims to establish a consensus among researchers on analyzing retinal blood flow data. By examining capillary-level changes in the eye, the research offers a noninvasive method to identify high-risk patients for cognitive impairment. The work highlights the potential of AI and machine learning in processing complex medical imaging data to improve early disease detection.

Note: This transcript has been lightly edited for clarity.

 You recently had a very interesting paper published. Can you give the name of that paper and the journal in which it was published?

, and the topic of the publication was using OCT-A angiography data in epidemiologic studies, especially as it relates to Alzheimer's and neurodegenerative diseases. So it's a very exciting and growing field, and I think it was a timely publication.

 Can you talk a little bit about how OCT-A is achieving this sort of biomarker look in the eye for Alzheimer disease and other conditions?

 So OCT-A, first of all, for and I think most people are starting to become familiar with it, but for anybody who isn't, OCT-A is a really excellent modality to measure capillary level perfusion in the eye. Because of the optics of the eye, we can do it noninvasively, which is hard to do in the brain, because you have to penetrate the skull with whatever modality. So things like MRI, PET scans, they just can't measure capillary-level blood flow. 

So with advent of OCT-A we can now measure blood flow in the retina, and the idea is that it's a proxy for perfusion in the CNS, in the intracranial space. This has become a very widely accepted idea that at least some aspects of pathology that occur in the brain for Alzheimer's disease, and perhaps for other diseases like vascular cognitive impairment, are reflected in the tissue of the retina. 

The question is, can we capture a picture of this, literally, in the retina, and hopefully tell us something more about what's happening in the intracranial disease process?

 In conducting this research, how was the study designed to analyze these photos and this data?

 The study that we published was really a first attempt at gaining consensus among a lot of stakeholders. So OCT-A has been around for about 10 years, and we were involved in the initial kind of FDA approval process with one of the main manufacturers and initial utilizations. So it hasn't been around that long. 

A lot of people have collected data, and one of the things we found is that it's a little bit tricky how you use those OCT-A data and how it's acquired. That's where really this consortium started to come together, is to try to get a handle of, "how do we do these analyses," so that one site in Europe and another site in Asia and the US, we can all get consistent interpretations of our data and make sure we're using the best data possible.

That was the motivation for this paper. What we did is we had a group of 7 or 8 universities that are running really large population-based studies and that have collected thousands and thousands of data sets from OCT-A, and we tried to get everybody around the table and say, "What is the best way of analyzing this data so that we don't have these differences?" 

Because right now, there are a lot of differences between published studies by group X and group Y. That was really the goal of this particular study: to get some consensus in terms of study design, analytical methods, and how do you use good quality data to generate the results that you want?

 Taking it one step further with more of a consensus among different stakeholders in the area, in the field, how might this apply to future technologies, whether we're talking about AI or whether we're talking about a large language model in the space?

 I think it has huge implications for how we collect data, because, one of the things that we've learned from one of the study sites, which was the Framingham Heart Study, was that, when you collect data from both eyes of an individual, we don't necessarily see the exact same correlation in the data between 2 eyes. That could be because of the way the data are collected, or it could be because of biological differences between blood flow to each eye. We're not absolutely sure about that. 

So a lot of times, people will a conductive study, and they'll dilate 1 eye, because they don't want to inconvenience the patient. Or, for example, in neurologic studies, the patient has to perform another task after the eye test. So if you dilate both, it can't be functional. It turns out that that may be an important variable. So if you just randomly dilate somebody, rather than systematically doing it, you may be introducing a bias one way or the other, or you may be missing something. So that's one thing we found at one of the sites.

I think the other things that we found are that how you collect these data, in terms of the size of the scans and how much of the retina you're looking at, makes a big difference in how we analyze them, because there are small vessels and there are large vessels, and there's small vascular disease and large vascular disease. Those things, I think, had been a little bit overlooked in the past, but I think that it's coming to to the forefront.

In terms of AI, the data sets that we're collecting, they're huge data sets, and these are large volumes, and we're just starting to get an appreciation for how these capillaries in the retina connect to each other and connect to large vessels. 

The role of AI and machine learning in analyzing these vascular patterns, I think, is going to be very important. We've already started developing software to remotely assess the quality of data at these different sites. One of the things that came through was that, you know, site X has 10,000 images that they need to review, and it's a very labor-intensive process, because you need somebody who's experienced in reading these images, and oftentimes, it's clinicians who are doing it, but they don't have time to read 10,000 images.

So one really active application of AI right now is to develop a method of looking through 10,000 images, picking the best ones for the analysis, and then leaving the rest as a secondary analysis, or saying, well, these may not give us as reliable results. That, in and of itself, is a big step forward, because all the sites were saying, we don't have a really great way of doing this.

 For the average ophthalmologist, or someone who's conducting these scans, looking at these scans on an individual level, what takeaways would you have for them as they start to incorporate this kind of research down the line?

 I think this is really exciting because it's putting ophthalmology perhaps in the driver's seat, or at least in a position where we can help our colleagues in neurology and even other specialties to risk-stratify patients. So I'm not so sure we're going to diagnose Alzheimer disease. 

I think our neurology colleagues are very good at that, but they're not very good at saying who is going to develop Alzheimer disease in the next 10 years, and who should we send for MRI testing or cognitive testing or PET scans, because each one of those tests is hard, much harder to do than OCT-A, which takes about 10 or 15 minutes, and for which you don't even have to dilate somebody. So MRIs are a couple hours and cost is very high. 

Cognitive testing requires a very experienced neuropsychologist to sit down an hour and a half of discussion back and forth. Language can be a barrier if the patient doesn't speak. You're not going to get good cognitive evaluations. PET scans require radiation to the body.

So, the issue is, how are you going to identify all these people to screen them? The other real practical implication is that when you want to do a clinical trial to try to find a treatment, you want to find a group of people who are at high risk for the disease, and you can't do an MRI on thousands and thousands and thousands of people. It's just not feasible. So hopefully we can provide a method for our neurology colleagues to say, hey, out of these 10,000 people, these 1000 are the highest risk group based on the scans that we've done. 

Let's try to focus on them and expand our really valuable resources on those groups of people.

 Are there any other areas you want to speak to, or anything you feel didn't get mentioned?

 It's really exciting to be able to look in the eye and assess capillary level changes in people who don't necessarily have a problem right now, but are on their way to developing a problem. We've done this now in a couple of different studies before this consortium, and I think that's where some of the interest is starting to arise. 

You know, when we look at people who have, for example, diabetes and hypertension, we notice that there's an increased chance that they have fewer capillaries or fewer areas of perfusion compared to people who are not diabetic and hypertension, and that may be reflecting an intracranial process as well. 

Similarly, we found people who have specific kinds of genetic mutations, even though they have no visual symptoms or cognitive symptoms, tend to have lower capillary density in their retina, which might mean that they're more predisposed to developing cognitive impairment in the future, whether from vascular disease or from Alzheimer. 

I think we're providing very useful information by looking at these subtle, but really important changes, in the eyes of people and trying to correlate them with their clinical and cognitive status from a neurology standpoint.

 Is there an age range with this kind of consensus looked at, or was it, you know, were we looking at a specific population of retirement age or younger?

 I think in general, cognitive impairment tends to be a problem, primarily in the [older] population. Alzheimer disease is the one we all traditionally think about, but stroke and vascular cognitive impairment, which is kind of not the typical stroke that we think of, but more microvascular, chronic stroke, are all really big problems, and it is very hard to distinguish those categories among the older groups. 

So that's primarily where we're interested, but we don't really know if this has applications earlier on, and it would certainly be interesting to study patients earlier to see if earlier causes of cognitive impairment are associated with it. I think we're pretty sure that we can pick out the vascular component of a disease process that is contributing to cognitive decline. 

The question is, how do we implement that in our studies, reliably and repeatedly, so that everybody can get the same results?

OCT-A angiography can help reveal early neurodegenerative disease signs, offering a noninvasive method for identifying high-risk patients through retinal analysis.

Canonical

clinical

Q&A: Amir Kashani on biomarkers for Alzheimer disease

A new study tackled the topic of drusen regression without accompanying atrophy and forwarded the “drusen ooze” hypothesis to explain this phenomenon (ie, that the content of the drusen moves to the subretinal space through defects in the retinal pigment epithelium [RPE]), which may explain 

 reported Jordi Monés, MD, PhD. He is affiliated with the Institut de la Macula, Centro Medico Teknon, and the Barcelona Macula Foundation, both in Barcelona, and the John A. Moran Eye Center, University of Utah, Salt Lake City.

He and his colleagues explained that although great strides have been made in the understanding of the biologic processes that precede the development of atrophy of RPE and photoreceptors, they recognized a subset of atrophy that results from the collapse of soft drusen, marking a crucial stage in disease progression.

“Although considerable attention has been focused on elucidating the mechanisms underlying drusen collapse and subsequent atrophy, a curious phenomenon has been poorly explained: drusen regression without accompanying atrophy. Despite its well-documented occurrence, it lacks a comprehensive explanation,"

They conducted this study to determine how often and why spontaneous soft drusen regresses without atrophy (DRwoA) in patients who had intermediate or atrophic 

The investigators retrospectively reviewed images from 640 consecutive eyes of 320 patients who had been followed for 2 years or longer. Among these, 427 eyes of 262 patients were identified who had intermediate or atrophic AMD and no present or past exudative AMD.

The main outcome measures were DRwoA with integrity of the RPE and repositioning over Bruch’s membrane; DCwA in the same area simultaneously referred to as “sentinel” DCwA; and the reversibility of features of incomplete RPE, outer retinal atrophy (iRORA), and the areas (“halos”) of DRwoA around the sentinel drusen.

Evaluation of the images obtained from the 427 eyes identified 53 occurrences of DRwoA, representing 24.17% of the eyes with soft drusen. In 50 of the cases (94.33%), a nearby sentinel DCwA was seen. In 58% of the cases, a well-identifiable halo of drusen disappearance around the sentinel DCwA was clearly visible, the investigators reported.

A previous study theorized that “drusen formation and reabsorption are dynamic processes that can occur concurrently in the macula.

In addition, the potential prognostic implications of drusen regression and its therapeutic implications for macular alteration have been pointed out."

Monés and colleagues explained that the most accepted hypothesis for the disappearance of drusen material during drusen regression “is reduced secretion by altered RPE, especially when it dies, causing it to stop producing drusen material and leading to the collapse of the drusen."

Those authors reported in a separate study that “RPE cells on the drusen apex either migrate into the retina or die, and the drusen collapses because the RPE is not present to maintain it.”

However, Monés and colleagues countered that the hypothesis does not explain drusen regression with the disappearance of drusen material with normal underlying RPE.

In the study under discussion, they identified a clear spatial and time relationship with DRwoA and DCwA, with at least 96% of the DRwoA having a close DCwA, and they occurred simultaneously, they said, indicating that both phenomena are related.

They explained further that in small soft drusen the connection may occur via a thin layer of drusen material, making the passage of material between drusen plausible, especially in low-density soft drusen, which has high fluid content, as represented by the drusenoid pigment epithelium detachment (PED) formed by coalescing drusen and accompanying surrounding soft drusen.

“The DRwoA around a collapsing drusenoid PED with atrophy is a typical phenomenon that can be observed in almost every case in daily practice to some extent. In drusen that will undergo DCwA, there invariably is an RPE defect at the apex of the drusen. This defect is a constant preceding stage in which hyperreflective dots are seen.

 On the other hand, this RPE defect allows the connection between the sub-RPE drusen material and the subretinal space and the inner retina circulation. A plausible pathway for this material could be via the deep vascular complex of the retina, especially given the way-out challenges of the thickened Bruch's membrane.”

Monés and colleagues previously reported features suggesting movement of drusen material into the subretinal space through defects in the RPE above the drusen, which they referred to as “drusen ooze.” Both the presence of the same isoreflective material on both sides of the RPE, through the RPE defects accompanying the hyperreflective dots, and heterogeneous hyperreflectivity in the drusen, suggested the movement of material from the drusen to the subretinal space.

Although they advised that the drusen ooze hypothesis is not intended to replace established mechanisms such as RPE cell death, macrophage involvement, and glial activation, it presents a complementary perspective, especially in cases with high fluid, low-density soft drusen.

Monés J, Pagani F, Santamaria JF, et al. Spontaneous soft drusen regression without atrophy and the drusen ooze. 

https://www.ophthalmologyretina.org/article/S2468-6530(25)00093-4/fulltext

Klein R, Klein BE, Tomany SC, et al. Ten-year incidence and progression of age-related maculopathy: the Beaver Dam eye study. 

Bressler NM, Munoz B, Maguire MG, et al. Five-year incidence and disappearance of drusen and retinal pigment epithelial abnormalities. Waterman study. 

Sparrow JM, Dickinson AJ, Duke AM, et al. Seven year follow-up of age-related maculopathy in an elderly British population. 

Sallo FB, Rechtman E, Peto T, et al. Functional aspects of drusen regression in age-related macular degeneration. 

Yehoshua Z, Wang F, Rosenfeld PJ, et al. Natural history of drusen morphology in age-related macular degeneration using spectral domain optical coherence tomography. 

Curcio CA. Soft drusen in age-related macular degeneration: biology and targeting via the oil spill strategies. 

Curcio CA, Zanzottera EC, Ach T, et al. Activated retinal pigment epithelium, an optical coherence tomography biomarker for progression in age-related macular degeneration. 

Schuman SG, Koreishi AF, Farsiu S, et al. Photoreceptor layer thinning over drusen in eyes with age-related macular degeneration imaged in vivo with spectral-domain optical coherence tomography. 

Ouyang Y, Heussen FM, Hariri A, et al. Optical coherence tomography-based observation of the natural history of drusenoid lesion in eyes with dry age-related macular degeneration. 

Researchers conducted this study to determine how often and why spontaneous soft drusen regresses without atrophy in patients who had intermediate or atrophic age-related macular degeneration.

New study examines soft drusen regression without atrophy and drusen ooze

A team of professors and researchers at the University of Houston has recently been awarded over $3.6 million by the National Institutes of Health’s National Eye Institute to investigate a gene in the eye that is crucial for normal vision but, when mutated, can cause retinal diseases that often lead to blindness. The gene, peripherin 2, has more than 300 variants when mutated as 

, which can cause diseases such as retinitis pigmentosa and macula-predominant disorders, including pattern dystrophy, cone-rod dystrophy, and several forms of macular degeneration, according to a news release.

When functioning properly, peripherin 2 is known to provide instructions for making a protein that shapes the outer segment of photoreceptor cells in the retina.

“We want to understand how defects with the 

gene lead to eye diseases,” said Muna Naash, PhD, John S. Dunn Endowed Professor of Biomedical Engineering, in the release. “Our main objective is to uncover the mechanisms underlying PRPH2-associated pathology, with a focus on its roles in rods and cones, the 2 types of photoreceptor cells in the retina.”

Naash will be working alongside Muayyad Al-Ubaidi, MD, John & Rebecca Moores Professor of Biomedical Engineering. “We will also examine how these cells are built and organized, and how proteins are transported to their outer segments,” said Naash in the release.

The release also noted that the underlying mechanisms of 

 are not currently well understood. Additionally, with so many mutations of the gene linked to eye diseases, 

is a research topic of concern for developing gene therapy.

“Despite considerable scientific advancement, there are still no clinically viable therapeutic options for 

retinal diseases,” Al-Ubaidi said in the release. “Gaining a thorough grasp of the mechanisms associated with 

diseases is crucial for designing effective therapies.”

Al-Ubaidi and Naash will be conducting their research by developing experimental models and various therapeutic platforms that will allow for the evaluation of disease mechanisms and test therapeutic strategies for 

“Our focus is to further explore the biochemical properties of 

 and its key binding partner, retinal OS membrane protein 1,” said Naash in the release. “This will aid our understanding of the precise mechanisms governing 

’s involvement in rod and cone outer segment rim formation, an elusive goal that has long hindered the development of effective therapies.”

Fickman L. University of Houston Biomedical Engineering researchers awarded $3.6 million to examine retinal diseases and blindness. University of Houston. September 10, 2025. Accessed September 10, 2025. 

https://www.uh.edu/news-events/stories/2025/september/09102025-biomedical-research-grant.php

Researchers will investigate a gene in the eye that is crucial for normal vision, but can cause retinal diseases when mutated that often lead to blindness.

University of Houston researchers receive $3.6 million to examine retinal diseases

Australian researchers identified in a recent study an association between 

 and cardiovascular disease (CVD): they showed that the presence of AMD predicted an increased risk of all-cause and CVD mortality in patients with a high risk of CVD, even in the early stages of AMD,

 according to Richard Kha, first author and medical student from the Centre for Vision Research, Westmead Institute for Medical Research, Westmead, New South Wales, Australia.

Kha was joined in this study by researchers from the Department of Cardiology, Westmead Hospital, Westmead, and the Department of Cardiology, Bankstown Hospital, Sydney, both in New South Wales, Australia.

The research team explained that while numerous studies have evaluated the relationship between AMD and CVD, no consensus was reached, and the results were inconsistent.

 Because there are no data that evaluated the impact of AMD on mortality in a high CVD risk cohort, they undertook a prospective cohort study that included 1545 patients who presented with acute coronary syndrome.

Importantly, they emphasized the high impact the 2 diseases have. AMD affects the central retina,

 resulting in an increased risk of falls,

CVD is the leading cause of mortality despite advances in cardiac diagnosis and management; it accounts for in excess of 30% of all deaths globally.

“It has been hypothesized,” they noted, “that AMD shares a similar risk profile to CVD.

 Many CVD risk factors that lead to shorter survival, such as advanced age, smoking, obesity, ethnicity, hypertension, and elevated serum cholesterol levels, are also associated with AMD.

All study patients underwent coronary angiography and fundus photography; the photographs were graded as any, early, or late AMD. The investigators’ stated goal was “to improve the current understanding of whether AMD is a useful prognostic indicator for identifying adults with a lower chance of survival in a population that already has a higher baseline risk of mortality. They hypothesized that patients with AMD in a high-risk cohort will have an increased risk of CVD-specific mortality.”

What was the relationship between AMD and CVD?

Kha and colleagues reported the presence of any AMD in 107 (6.9%) participants, including those with early (n = 86) and late AMD (n = 21).

“Over 9 years of follow-up, 234 (15.1%) participants had died, including 174 (11.3%) participants from fatal CVD events. After controlling for age, sex, body mass index, total cholesterol, smoking status, history of diabetes, hypertension, myocardial infarction, stroke, and macrovascular coronary artery disease severity using the Gensini score, there was an increased rate of all-cause mortality for those with any AMD (HR, 2.37; 95% CI, 1.54–3.64), early AMD (HR, 2.42; 95% CI, 1.48–3.94), and late AMD (HR, 2.25; 95% CI, 1.08–4.71),” they said.

They also found that any AMD (HR, 2.62; 95% CI, 1.61–4.26) and early AMD (HR, 2.61; 95% CI, 1.50–4.64) were also associated with a greater likelihood of CVD mortality. However, late AMD was not associated with CVD mortality.

Currently, the mechanisms underlying the association between AMD and CVD mortality are not clear.

“It is possible that AMD shares common antecedents with macrovascular diseases such as CVD. Chronic inflammation, oxidative stress, atherosclerosis, and abnormal lipid homeostasis are common biological mechanisms implicated in the development of AMD and CVD.

 In AMD, oxidative stress, inflammation, and complement pathway activation lead to retinal pigment epithelial cell death and drusen formation.

 Drusen consist of lipids and apolipoproteins, and the mechanism behind drusen formation is thought to be similar to that of atherosclerotic plaques.

 Oxidized lipids interact with macrophages, initiating an inflammatory cascade resulting in atherosclerosis.

 The excessive formation of arterial plaques increases the risk of adverse CVD events, such as stroke or fatal myocardial infarction,” the authors theorized.

Other factors are the strong association between genetic variants of complement factors and the development of AMD,

 and the activation of the complement pathway that predicts CVD and stroke risk.

 In the systemic vasculature, interactions between oxidative stress, inflammation, and atherosclerosis lead to CVD and its adverse events.

 In addition, the presence of reticular pseudodrusen, which is linked with the Y402H and ARMS2 69S alleles, has also been found to be associated with CVD and higher mortality rates.

The authors concluded, “AMD is a complex multifactorial disease that shares similar processes with CVD, and the association between AMD and CVD mortality is likely to be a combination of multiple factors rather than a single shared risk factor or biological pathway. Future research should seek to clarify the impact of reticular pseudodrusen and genetic variations in the complement pathway on AMD and CVD events.”

Kha R, Burlutsky G, Thiagalingam A, et al. Association between age-related macular degeneration and mortality in a high cardiovascular risk cohort: a prospective cohort study. 

https://www.ophthalmologyretina.org/article/S2468-6530(25)00094-6/fulltext

Gopinath B, Liew G, Burlutsky, G, et al. Age-related macular degeneration and risk of total and cause-specific mortality over 15 years. 

Fisher DE, Jonasson F, Eiriksdottir G, et al. Age-related macular degeneration and mortality in community-dwelling elders: the age, gene/environment susceptibility Reykjavik study. 

Tan JS, Wang JJ, Liew G, et al. Age-related macular degeneration and mortality from cardiovascular disease or stroke. 

The presence of AMD predicted an increased risk of all-cause and CVD mortality in patients with a high risk of CVD, even in the early stages of AMD.

Sponsored by Bayer

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