About one in three people over the age of 80 experience age-related macular degeneration (AMD), a condition that affects the retina and leads to loss of central vision. In the United States, approximately 20 million adults age 40 and older are currently living with AMD. The vast majority have the “dry” form, which develops gradually and eventually causes difficulty in seeing objects directly in front of them. Despite being one of the most common causes of vision impairment among the elderly, there is still no effective treatment for dry AMD.
Researchers at Aalto University have identified a promising new way to slow or even stop the early stages of dry AMD. Their approach focuses on strengthening the retinal cells’ natural defense systems by applying controlled heat, according to Professor Ari Koskelainen.
“Cellular functionality and protective mechanisms weaken with age, which exposes the fundus [the inside surface at the back of the eye] to severe oxidative stress,” explains Koskelainen. “Oxygen free radicals damage the proteins, which causes them to fold and clump, and then fatty protein deposits called drusen begin to accumulate, which is the main diagnostic criterion for the dry form of age-related macular degeneration.”
Using heat to trigger the eye’s repair response
Treatment involves carefully warming the affected tissue by several degrees, a difficult task because it is difficult to measure the temperature behind the retina. Temperatures above 45 degrees Celsius can damage the tissue, but Aalto’s team developed a method that allows real-time temperature monitoring while heating the area with near-infrared light. This allows for safe, precise control when using heat to activate the eye’s natural healing responses at the cellular level.
When proteins inside the eye misfold, cells can respond in a number of ways. One mechanism involves heat shock proteins, which are produced in response to stress and can help refold damaged proteins to their original structure. If this process fails, the defective proteins are targeted for breakdown into amino acids so they can be recycled.
If protein aggregation has already occurred, another mechanism called autophagy takes over. This process, discovered by Nobel laureate Yoshinori Ohsumi in 2016, involves clustering within a lipid membrane similar to a cell membrane. Recognition proteins on the surface of the membrane signal lysosomal enzymes to begin breaking down and removing the damaged material.
“We were able to show that we can activate not only the production of heat shock proteins, but also autophagy using heat shocks. This process is similar to the disposal of waste,” says Koskelainen.
Promising results and next steps
The new technique has already produced positive results in animal studies involving mice and pigs. Human clinical trials are scheduled to begin in Finland in the spring of 2026. The first phase will focus on confirming the safety of the laser treatment before moving on to determine how often it should be repeated for lasting results.
“Treatment must be repeated, as the response can already start to decline a few days after treatment,” says Koskelainen.
The findings were published in Nature communications on October 29. The research team also created a spin-off company, Maculaser, to help bring the treatment into clinical use.
“An optimistic plan would see the method already in use in hospital eye clinics in just three years,” adds Koskelainen. “The ultimate goal is to have it readily available at your local eye doctor.”
