
Age-related macular degeneration, often called AMD, is one of the leading causes of vision loss in older adults.
The disease affects the macula, a small but extremely important part of the retina that helps people see clearly in the center of their vision.
The macula allows people to read, drive, recognize faces, and perform many everyday tasks. When it becomes damaged, vision can slowly fade and, in severe cases, people may lose much of their central sight.
AMD is a growing global health problem because people are living longer than ever before. In Australia, around one in seven people over the age of 50 are affected by the condition.
Worldwide, scientists estimate that more than 196 million people live with AMD. As populations continue aging, the number is expected to rise sharply in the coming decades.
There are different stages of AMD. Some people experience only mild vision changes for many years, while others rapidly develop severe damage that can lead to major sight loss.
Doctors currently have only limited treatment options. Existing treatments mainly slow the disease after serious damage has already started, and not all patients respond well to these therapies.
Now, a major new study from researchers at the University of Melbourne, the Center for Eye Research Australia (CERA), and the Garvan Institute of Medical Research has uncovered important biological differences that may explain why some people develop more severe forms of AMD than others.
The findings were published in the scientific journal Genome Medicine. Researchers believe the discovery could eventually lead to more personalized treatments designed for different types of AMD.
The scientists focused on a particular form of AMD linked to unusual deposits in the retina called reticular pseudodrusen. These deposits are associated with a much higher risk of severe disease and vision loss.
Patients with reticular pseudodrusen are more likely to progress to advanced AMD, but until now, scientists did not fully understand why.
To investigate the problem, the research team collected skin biopsies from more than 100 Australians living with AMD. Some participants had reticular pseudodrusen, while others had more typical forms of the disease.
Using advanced stem cell technology, the scientists transformed the skin cells into retinal cells in the laboratory. This allowed them to closely study how the cells behaved and compare the biological activity between the two groups.
The researchers examined which genes and proteins were active inside the retinal cells. Genes act like instruction manuals for cells, while proteins help carry out the cell’s daily functions.
By studying these molecular differences, the team hoped to uncover what makes severe AMD different from the more common form of the disease.
The results showed that patients with reticular pseudodrusen had important biological differences in their retinal cells.
According to Professor Alice Pébay from the School of Biomedical Sciences and Melbourne Medical School, the severe form of AMD appeared to involve stronger activity in processes linked to cell support, structure, and stability.
This means that even though different forms of AMD may appear similar during eye examinations, they may actually develop through different biological pathways inside the body.
Professor Pébay explained that not all AMD is biologically the same. This finding is important because it suggests that treating all patients in the same way may not be the best approach.
Co-lead author Professor Robyn Guymer, Deputy Director of CERA, said the study helps explain why current treatments do not work equally well for all patients. Some people respond to treatment while others continue losing vision, and the newly discovered biological differences may partly explain this problem.
The findings support a growing idea in medicine called precision medicine. Instead of treating all patients with the same therapy, doctors try to match treatments to the specific biology of each patient’s disease.
This approach is already being used in some cancers and genetic diseases, and researchers now hope it may improve treatment for AMD as well.
The study also demonstrates how stem cell technology is changing medical research. By turning ordinary skin cells into retinal cells, scientists can study eye disease in ways that were impossible in the past. This allows researchers to better understand disease processes without needing to directly remove cells from the eye.
Although the research is still at an early stage, experts say it represents an important step forward. Understanding the exact biological pathways involved in severe AMD could eventually help scientists design new drugs that target the disease more precisely and possibly prevent severe vision loss before it occurs.
The study findings appear strong because the researchers used advanced molecular analysis and examined samples from a relatively large group of patients. However, further research is still needed to confirm the results and determine how these discoveries can be translated into real treatments.
The research also highlights the complexity of AMD. For many years, AMD was often treated as a single disease, but the new findings suggest it may actually include several related conditions with different underlying causes.
If future studies continue supporting these results, doctors may one day be able to identify which patients are at highest risk of severe AMD much earlier and provide more targeted care. This could greatly improve outcomes for millions of people at risk of losing their vision as they age.
If you care about eye health, please read studies about how vitamin B may help fight vision loss, and MIND diet may reduce risk of vision loss disease.
For more information about eye disease, please see recent studies about how to protect your eyes from glaucoma, and results showing this eye surgery may reduce dementia risk.
Source: University of Melbourne.


