New macular degeneration treatment the first to halt disease’s progression

Around a third of people over the age of 80 suffer from age-related macular degeneration (AMD), with an estimated 20 million Americans aged 40 and older currently living with AMD. The majority of cases are the dry form of the disease, which progresses slowly, eventually resulting in sufferers losing the ability to see objects that are directly in front of them. Yet despite its prevalence, there is no effective treatment for dry AMD.

Now, Aalto University researchers have uncovered a promising way to treat the dry form of the disease in the early diagnosis phase that could potentially stop its progression. The novel treatment approach aims to strengthen the protective mechanisms of affected cells using heat, explains 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 intense oxidative stress,’ he explains. ‘Free oxygen radicals damage proteins, which causes them to misfold and aggregate, then fatty protein deposits called drusen begin to accumulate, which is the main diagnostic criterion for the dry form of age-related macular degeneration.’

The approach requires heating the tissue by several degrees, which is complicated, as it’s hard to measure the temperature behind the retina, and temperatures above 45 degrees Celsius can cause tissue damage. The newly developed method allows for temperature monitoring at the same time as heating is carried out with near infrared light. Koskelainen says, amongst other benefits, it harnesses the power of heat to trigger healing responses at a cellular level.

Misfolded proteins can be treated in three different ways. Heat shock proteins, which are produced by cells in response to environmental stress, can repair them to their original shape. If this does not work, the misfolded proteins are primarily directed to be broken down into amino acids.

If accumulations have already formed, a process called autophagy comes into play, the discovery of Yoshinori Ohsumi, who was awarded the Nobel Prize in Medicine for the discovery in 2016. In this process, a lipid membrane similar to a cell membrane is built around the accumulation, with recognition proteins on its surface. With the help of these proteins, lysosomal enzymes begin to break down aged and damaged proteins.

‘We were able to show that we can activate not only the production of the heat shock proteins, but also autophagy using the heat shocks. This process is similar to waste disposal,’ says Koskelainen.

The method has been shown to work in mice and pigs, and patient trials will start in Finland in spring 2026. The first phase of the trials will ensure the safety of the treatment approach in humans, without yet seeking a therapeutic response. Researchers then hope to progress towards establishing how often the treatment would need to be repeated.

‘The treatment needs to be repetitive, since the response can already begin to decline some days after the treatment,’ Koskelainen says.

The research was first published in Nature Communications on 29 October. Meanwhile, researchers aim to commercialise the discovery, and have established a research-to-business start-up called Maculaser.

‘An optimistic schedule would see the method already being used in hospital eye clinics in as little as three years’ time,’ says Koskelainen. ‘The eventual goal is that it would be readily available at your local ophthalmologist.’