Age-related macular degeneration (AMD), one of the leading causes of blindness among older people in rich countries, may eventually be treated by restoring the eye’s natural cellular recycling system, according to research led by the University of Fribourg.
As populations age, retinal diseases are becoming increasingly common worldwide. AMD damages two types of cells that are essential to vision: photoreceptors, which detect light, and retinal pigment epithelial cells, which support and nourish them. Over time these cells accumulate damaged proteins and other waste products.
Under normal conditions cells dispose of such material through internal cleaning mechanisms. But these systems weaken with age. Waste accumulates, cells become stressed and vision gradually deteriorates. Researchers believe that understanding why these mechanisms fail could eventually help slow—or perhaps prevent—the progression of degenerative eye diseases.
A team led by Patricia Boya of the University of Fribourg, working with American and Spanish collaborators, focused on a process known as chaperone-mediated autophagy (CMA). In this system specialised proteins, known as chaperones, identify damaged proteins and transport them to lysosomes, the structures responsible for breaking down and recycling cellular waste.
The researchers found that CMA is particularly active in retinal cells, where it acts as a form of quality control. When the mechanism malfunctions, as it appears to do in patients with AMD, defective proteins accumulate and retinal cells lose their ability to function properly.
The scientists also showed that the process could be reactivated using an experimental molecule known as CA77.1, designed to stimulate this cellular recycling pathway. In laboratory models activation of CMA reduced waste accumulation, limited inflammation and slowed the deterioration of vision.
The team, which also included Jörn Dengjel of the University of Fribourg’s Department of Biology, tested the approach on cells derived from AMD patients. The results suggested that strengthening the cell’s internal cleaning system helped restore cellular balance and improved resistance to stress.
The research remains at an early stage. But the approach is attracting interest because it targets a broader mechanism associated with cellular ageing rather than focusing on a single symptom or pathway. By helping retinal cells clear waste more efficiently, researchers hope future therapies could slow—or potentially prevent—vision loss linked to ageing.
For millions at risk of AMD, that prospect offers cautious grounds for optimism.
Age-related macular degeneration affects roughly one in ten people over the age of 50, although most cases are mild and detected at an early stage. More advanced forms of the disease, which threaten central vision, affect around 1-2% of over-50s. The prevalence of AMD rises sharply with age. Around 2% of people aged 40-44 show signs of the condition. By the late 60s the figure is closer to 10%. Among those over 80, some studies suggest that more than a quarter are affected.
More on this:
University of Fribourg article (in English)
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