The Future of Fighting Disease May Start Before We Feel Sick

Everyone knows prevention is better than treatment. The hard part is making that idea work in real medicine and for real people, at scale.

At the 75^th Lindau Nobel Laureate Meeting, three Lectures pointed toward a very different medical future, one in which disease can be detected before symptoms appear, or where the body can be given instructions and the immune system can be tweaked with precision.

The speakers came from different corners of science: Ferenc Krausz, a physicist; Katalin Karikó, an mRNA pioneer; and Shimon Sakaguchi, an immunologist. But together, they hinted at the same shift. Medicine is moving away from waiting for the body to break down and starting to look for the earliest signs that something is going wrong.

Reading disease before it speaks

Ferenc Krausz is not a physician. He’s a physicist who learned how to measure some of nature’s fastest motions.

Born in Hungary, Krausz became one of the pioneers of attosecond physics, a field that uses flashes of light lasting billionths of a billionth of a second to study how electrons move in atoms and molecules. In 2023, he shared the Nobel Prize in Physics with Pierre Agostini and Anne L’Huillier for experimental methods that generate attosecond pulses of light to study electron dynamics in matter.

Now, Krausz is trying to bring tools born in ultrafast physics into medicine.

He began his lecture in the Lindau Inselhalle with one of the hottest topics in healthcare: artificial intelligence. AI is already being tested across medicine, from image analysis to diagnosis. But Krausz emphasized a basic limitation.

“Data and AI may revolutionize healthcare, but I would argue that AI can only be as good as the data used for training,” Krausz says.

That is the catch. Much of today’s medical AI is trained on data from people who are already patients. They have symptoms or abnormal scans and may already have a diagnosis. That kind of data can help an algorithm recognize established disease but it is less useful for prevention, because prevention requires seeing the body before disease becomes obvious.

Krausz’s idea is to look earlier, and to look differently.

Instead of using visible light to follow electrons, his team uses infrared light to “read” blood. In this approach, blood plasma is exposed to infrared pulses that make molecules vibrate. Those vibrations create a signal, almost like a molecular fingerprint. Infrared molecular fingerprinting can capture broad information from a blood sample, and studies have shown that these fingerprints can be stable enough within individuals to make long-term monitoring plausible.

As Kraus put it, “This solution was looking for a problem,” and the problem became obvious when the AI data limitations were considered.

His idea has two parts. First, collect data earlier: repeated blood samples from people while they are still apparently healthy. Second, make the comparison personal. Instead of asking whether your blood looks abnormal compared with the population, ask whether it has drifted away from your own baseline.

Because this testing method offers so many data signals at once (and does so affordably), it’s excellently suited for training AI. The AI outputs are then more meaningful because the data is longitudinal and pre-symptomatic. Krausz said early detection will require medicine to move beyond one-time tests, though that shift, he cautioned, will demand “a new clinical study design” built around repeated sampling rather than today’s symptom-guided care.

Krausz also has some preliminary results to back this idea up. His team has already recruited nearly 13,000 people and collected more than 73,000 blood plasma samples. Analyzing this data, they found one variable that appeared to warn of a cardiovascular condition two years before diagnosis, while another infrared variable signaled Type 2 diabetes 2.3 years before conventional markers suggested a problem.

Using the body’s own messengers

It is hard to imagine a more inspiring scientific journey than Katalin Karikó’s.

In her Lindau Lecture, she recalled growing up in Hungary in an adobe house with one room and no running water. Her father was a butcher, and from him she learned the value of hard work.

“That, and how to make sausages,” she joked.

In highschool, Karikó wanted to become a scientist even though she had never met one in her hometown of about 10,000 people. A book on stress changed the way she thought about pressure and ambition. One lesson stayed with her: focus on what you can change, even when things get tough.

“I wouldn’t be standing here if I had not read this book when I was 16,” she said. “And let me tell you that everyone feels stress, including Nobel Laureates.”

That stoic philosophy made all the difference in her career.

For decades, Karikó worked on messenger RNA at a time when many scientists saw it as a fragile, impractical molecule. Granted, the idea was powerful and elegant. DNA stores genetic information while messenger RNA carries instructions from DNA to the cell’s protein-making machinery. If scientists could deliver the right mRNA into cells, the body could temporarily make a useful protein. But turning that idea into medicine was brutally difficult.

It turned out that mRNA breaks down easily and is very hard to deliver into cells. Early versions could trigger unwanted inflammation. For years, the field struggled to attract attention and funding. “Every year there was just one publication out,” Karikó recalled.

When she later met some of the scientists who had published those early papers, she asked why they had not continued. The answer was always that they didn’t get funding. Karikó herself struggled to get funding. She faced demotions, job loss, and great skepticism from her peers.

She described herself as an outsider. “I didn’t get the money, nothing,” she said. “I [was] an outsider. I had just one advantage. I had freedom.”

That freedom is what eventually got us the mRNA breakthroughs that brought the first COVID vaccines. In 1997, she met Drew Weissman, who wanted to develop vaccines. Karikó recalled how she told him that she worked with RNA and offered to make RNA for him.

That collaboration continued and, ultimately, brought about Nobel-winning research. Together, the two confronted one of the key obstacles to mRNA medicine: eliminating the inflammation problems that typically came with mRNA. Karikó recalled the adversity she faced, but circled back to her stoic philosophy that made it all possible.

“If you want to do something, you find a way; if not, you find excuses,” she said.

The COVID-19 vaccines later made mRNA famous. But Karikó’s Lecture emphasized that the platform is still expanding, and the applications are already being explored in the clinic.

There are over 150 clinical trials currently ongoing, the Laureate mentioned. Some of them focus on infectious diseases or parasites, while others focus on cancer vaccines, including personalized cancer vaccines. The applications of mRNA-based therapies also include cardiovascular diseases, diabetic wounds, genetic diseases, and CAR T cells.

Not too bad for an outsider from an adobe house.

Telling the body when not to attack

Shimon Sakaguchi is also interested in the immune system; but he’s more interested in when the immune system goes too far and has to be stopped.

 “Our immune system, it has a very exquisite and very efficient way of protecting our body from invading microbes,” he said. “However, if this immune system turns against our own tissue, it is disastrous. It causes autoimmune diseases.”

Approximately 10% of the population is afflicted with some sort of autoimmune diseases, including multiple sclerosis, type 1 diabetes, thyroid disease, lupus, rheumatoid arthritis, and inflammatory bowel disease. They all share a frightening feature: the body’s defenses begin to attack the body itself.

For a long time, immunologists struggled to understand how the immune system avoids this fate most of the time. Sakaguchi helped reveal an important part of the answer: regulatory T cells, or Tregs.

These cells act like brakes on the immune system. They help restrain immune attacks and prevent self-reactive immune cells from damaging healthy tissue. In 2025, Sakaguchi shared the Nobel Prize in Physiology or Medicine with Mary Brunkow and Fred Ramsdell for discoveries related to peripheral immune tolerance, the process that keeps the immune system from attacking the body’s own tissues.

Sakaguchi showed that removing a small group of T cells from mice could unleash autoimmune disease. Restoring those cells could prevent it. Later work, including discoveries involving the FOXP3 gene, helped confirm that regulatory T cells are a distinct and essential immune population. FOXP3 mutations are linked to severe immune disorders, including IPEX syndrome in humans.

The implication is profound. It means that the immune system stays safe not because every dangerous cell has been eliminated, but rather because these cells are actively restrained. This, in turn, means that the border between self and non-self is not fixed, but movable.

The consequences go beyond autoimmune disease. In cancer, regulatory T cells can sometimes suppress immune attacks that might otherwise destroy tumors. In transplantation, strengthening regulatory T cells could help the body tolerate a new organ without lifelong broad immune suppression. Sakaguchi described mouse experiments in which expanding naturally present regulatory cells induced transplant tolerance without suppressive drugs.

Now, the next therapeutic frontier is balance. You don’t want to deplete Tregs everywhere, because autoimmunity may follow. But if you expand them too broadly, immunity against cancer or infection may weaken. The goal is then to learn when and how to best tune the body’s immune system.

Together, the three Lectures presented a promising view where medicine is increasingly built on information and pre-empting problems. Krausz wants to read the molecular signals in blood before disease becomes obvious. Karikó’s mRNA sends cells instructions. Sakaguchi’s Tregs help decide whether the immune system attacks or stands down.

All of these approaches come with challenges and problems, of course, but the potential is encouraging. The future of fighting disease may not be defined only by stronger drugs or more aggressive drugs or surgeries. It may depend on catching biological change sooner, delivering more precise instructions and learning to adjust the body’s own defenses.