Surreal illustration of an eye transforming into a landscape, symbolizing macular degeneration research.

Vision Breakthrough: Can We Slow Macular Degeneration?

"New research highlights a potential way to reduce vision loss by targeting a specific enzyme. Could this be the key to slowing AMD?"


Age-related macular degeneration (AMD) is a major concern, impacting central vision for millions worldwide. Characterized by the deterioration of the macula, the central part of the retina, AMD makes everyday tasks like reading and driving increasingly difficult. While there are treatments to manage the condition, finding ways to slow or prevent its progression remains a top priority for researchers.

A new study offers a promising lead, focusing on choroidal neovascularization (CNV), a key process in wet AMD. CNV involves the growth of new, leaky blood vessels under the retina, leading to swelling and vision loss. Researchers have been working hard to understand what triggers CNV and how to stop it.

This article unpacks the findings of a recent scientific paper that explores the role of serine racemase, an enzyme, in the development of CNV. We will explore how inhibiting this enzyme could potentially reduce the severity of AMD and preserve vision.

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AMD in the United States

The CDC identifies the Vision and Eye Health Surveillance System (VEHSS) modeled estimate as its primary estimate of age-related macular degeneration prevalence in the United States. For its 2019 estimates, VEHSS researchers used Bayesian meta-regression to combine information from multiple data sources and modeled AMD prevalence across the entire U.S. population. AMD becomes more common with age, and the growing older population is contributing to a larger number of affected people.

From Terminology to Treatment

Historical accounts show that AMD was described using terms such as senile macular chorioretinal degeneration and senile macular degeneration. The 2016 historical analysis notes that a clear disease concept is important for conducting sound epidemiologic and genetic research. Later treatment history centered on anti-VEGF therapies, while tyrosine kinase inhibitor treatments entered clinical trials as potential future approaches.

Serine Racemase: A New Target for Vision Protection?

Surreal illustration of an eye transforming into a landscape, symbolizing macular degeneration research.

The recent study shines a spotlight on serine racemase (SR), an enzyme present in the retina. SR is responsible for producing D-serine, which acts as a co-agonist of the N-methyl-D-aspartate receptor (NMDAR). When this receptor is activated, it boosts the production of nitric oxide (NO), a molecule known to promote both retinal and choroidal neovascularization. This discovery suggests that SR could play a vital role in CNV.

To investigate this connection, researchers examined mice with laser-induced CNV. The findings revealed that inactivating the SR-coding gene (Srrnull) significantly reduced CNV volume, decreased neovascular density, and limited the invasion of macrophages—immune cells that contribute to inflammation and blood vessel growth.

  • Reduced CNV volume
  • Decreased neovascular density
  • Limited macrophage invasion
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Oxidative Stress and New Targets

Recent research examined how oxidative stress affects LAMTOR1 in retinal pigment epithelium, using menadione (VK3) and 4-hydroxynonenal (4-HNE) as stressors. The study observed reduced LAMTOR1 in both human and mouse retinal pigment epithelium after short-term exposure of 1 hour and prolonged exposure of 24 hours. Other research identified 30 key genes, six miRNAs, and four lncRNAs in a molecular network related to exudative AMD, while reviews describe efforts to prevent degeneration and repopulate the atrophic macula.

Persistent Treatment Barriers

Reviews describe AMD as a progressive disease that remains a major cause of irreversible blindness in developed countries. They also warn that an aging population is expected to increase the number of cases, making effective solutions an urgent socioeconomic need. Drug delivery remains difficult because posterior segment barriers obstruct access to the retina and macula.

Treatment Depends on Disease Type

Treatment choices differ according to the type of macular degeneration. Wet AMD is treated with anti-VEGF drugs delivered through regular eye injections, and these medicines can stabilize or improve vision in many patients. The American Academy of Ophthalmology compares four commonly used anti-VEGF drugs for wet AMD, while Stargardt disease has no established treatment and myopic macular degeneration may also have a wet form treated with anti-VEGF drugs.

Further experiments explored the impact of SR inactivation on inducible nitric oxide synthase (iNOS) and vascular endothelial growth factor receptor 2 (VEGFR2). The results indicated that choroid/RPE homogenates from laser-injured Srrnull mice had less iNOS and decreased phospho-VEGFR2 compared to wild-type mice. In vitro studies further confirmed these findings, showing that inflammation-primed wild-type RPEs expressed more iNOS and produced more NO and VEGF than inflammation-primed Srrnull RPEs. When co-cultured with inflammation-primed Srrnull RPE, fewer choroidal endothelial cells migrated, suggesting that SR deficiency reduces RPE response to laser-induced inflammatory stimuli.

Hope for the Future

These findings offer hope for new treatments to slow down or prevent vision loss from AMD. By targeting serine racemase, researchers may be able to reduce the harmful effects of CNV and preserve eyesight. Further research is needed to translate these discoveries into effective therapies, but this study marks a significant step forward in the fight against AMD.

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Opportunities and Challenges in 2025

A 2025 special issue of Eye on AMD brought together articles and reviews from field leaders on the current status of age-related macular degeneration. Its focus included future opportunities as well as challenges facing the field. This framing places AMD research within an ongoing effort to assess present progress while identifying unresolved barriers.

From Trials to Daily Care

Recent real-world studies have examined how AMD treatments perform outside controlled trials. One study reported on real-world use of intravitreal pegcetacoplan for geographic atrophy, while another evaluated one-year anatomic and functional outcomes after treatment-intensive patients with neovascular AMD switched to faricimab. A separate study addressed poor adherence and treatment discontinuation by evaluating a structured patient engagement program for people receiving anti-VEGF therapy.

About this Article -

Written with AI assistance from published research, and reviewed by the Mystum team. See our About page for more information.

This article is based on research published under:

DOI-LINK: 10.1111/jnc.14214, Alternate LINK

Title: Serine Racemase Deficiency Attenuates Choroidal Neovascularization And Reduces Nitric Oxide And Vegf Levels By Retinal Pigment Epithelial Cells

Subject: Cellular and Molecular Neuroscience

Journal: Journal of Neurochemistry

Publisher: Wiley

Authors: Haiyan Jiang, Mengjuan Wu, Yimei Liu, Liping Song, Shifeng Li, Xianwei Wang, Yun-Feng Zhang, Junxu Fang, Shengzhou Wu

Published: 2017-10-13

Everything You Need To Know

1

What exactly is age-related macular degeneration (AMD)?

Age-related macular degeneration (AMD) is an eye disease that affects the macula, the central part of the retina. This deterioration leads to a loss of central vision, making it difficult to perform tasks like reading and driving. AMD is a leading cause of vision loss for older adults.

2

Can you explain what choroidal neovascularization (CNV) is and why it is important?

Choroidal neovascularization (CNV) is the growth of new, abnormal blood vessels under the retina. These vessels are often leaky, causing swelling, bleeding, and ultimately, vision loss. CNV is a significant factor in wet AMD, a more severe form of the disease, where the rapid growth of these blood vessels accelerates vision decline. Understanding and controlling CNV is critical in managing AMD.

3

What is the role of serine racemase in the context of vision loss?

Serine racemase is an enzyme that produces D-serine, which then activates the N-methyl-D-aspartate receptor (NMDAR). When NMDAR is activated, it increases the production of nitric oxide (NO). Nitric oxide promotes both retinal and choroidal neovascularization. Therefore, serine racemase plays a role in the development of CNV and, consequently, in the progression of AMD.

4

What happens when serine racemase is inactivated in the context of AMD?

Inactivating the serine racemase-coding gene (Srrnull) in studies led to several positive outcomes. These included a reduction in CNV volume, decreased neovascular density, and limited invasion of macrophages. Furthermore, there was less inducible nitric oxide synthase (iNOS) and decreased phospho-VEGFR2. These results suggest that reducing serine racemase activity could mitigate the development and severity of CNV, offering a potential therapeutic strategy for AMD.

5

How could targeting serine racemase lead to new treatments for AMD?

Targeting serine racemase offers a new avenue for potential treatments for AMD by reducing the harmful effects of CNV. This approach could help preserve eyesight by slowing down or preventing the progression of vision loss. While further research is necessary to develop effective therapies, the initial findings indicate that inhibiting serine racemase could have a significant impact on managing AMD.

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