Now, researchers at Columbia University have uncovered a biological mechanism that could help explain this remarkable resistance. Their findings point to a rare genetic mutation that protects the brain’s blood vessels from damage, potentially opening a new path toward Alzheimer’s treatments.

The discovery builds on research the team published two years ago involving APOE ε4, a gene variant strongly associated with Alzheimer’s risk. The scientists found that some people carrying APOE ε4 also possess a rare protective mutation in the fibronectin (FN1) gene.

Fibronectin is a protein that helps support the structure of tissues. However, in people with APOE ε4, excessive amounts can accumulate around blood vessels in the brain, potentially compromising a critical protective system known as the blood-brain barrier. The rare FN1 mutation appears to limit this buildup and the damage associated with it.

That earlier discovery suggested an intriguing possibility: What if scientists could develop a treatment that recreates the protection provided by this rare mutation?

A new study published in Nature Aging brings that possibility closer by identifying how excess fibronectin damages the brain’s protective barrier and revealing potential ways to interrupt the process.

“This new study takes us from a genetic clue to a disease mechanism,” says Caghan Kizil, the study’s corresponding author and professor of neurological sciences in the Department of Neurology and the Taub Institute for Research on Alzheimer’s Disease and the Aging Brain at Columbia University Vagelos College of Physicians and Surgeons.

“We knew that changes in fibronectin could protect against Alzheimer’s, but we didn’t know why excess fibronectin was harmful in the first place. This study gives us that detailed mechanism — and with it, ideas for how to reproduce that natural protection.”

How an Alzheimer’s Risk Gene Weakens the Blood-Brain Barrier

The blood-brain barrier serves as a protective boundary between the bloodstream and the brain. Made up of tightly connected cells surrounding the brain’s blood vessels, it carefully regulates which substances can enter brain tissue while helping maintain conditions necessary for removing potentially harmful waste.

When this barrier becomes damaged or excessively permeable, substances that would normally be kept out can enter the brain more easily. Such disruptions may contribute to inflammation and other processes involved in neurological diseases, including Alzheimer’s.

To investigate the role of fibronectin, the Columbia team combined several advanced research approaches. They examined human brain tissue and cerebrospinal fluid, the clear liquid surrounding the brain and spinal cord, using genetic and epigenetic analyses to explore changes in DNA and gene activity.

Their investigation also included single-cell sequencing, which reveals the activity of individual cells, and spatial imaging to examine where biological changes occur within tissues. Additional experiments involved human stem-cell models, three-dimensional cultures of blood vessels, and studies in zebrafish and mice.

Despite the variety of methods, the findings consistently pointed to the same mechanism: APOE ε4 promotes the production and accumulation of fibronectin around the brain’s blood vessels.

In mice engineered to carry human APOE ε4, researchers measured nearly twice as much fibronectin in the brain as in mice carrying APOE ε3, another common version of the gene. The greater accumulation was accompanied by evidence that the blood-brain barrier had become leaky.

Scientists Discover How Fibronectin Causes Brain Damage

One experiment provided especially important evidence that fibronectin does more than simply accumulate in damaged blood vessels.

The researchers increased human fibronectin specifically in astrocytes, specialized support cells that help maintain the blood-brain barrier and keep the brain functioning properly.

Increasing fibronectin in these cells was enough to disrupt the barrier, allowing it to become more permeable. Conversely, reducing fibronectin improved the barrier’s ability to function normally.

These results provided experimental evidence that excess fibronectin can directly contribute to blood-brain barrier damage rather than merely appearing alongside it.

“The animal experiments allowed us to move beyond association,” says co-first author Prabesh Bhattarai, an associate research scientist in the Kizil lab. “When we increased fibronectin in astroglia, the barrier became permeable. When we reduced fibronectin, barrier function improved.”

The team then investigated the molecular events responsible for the damage.

They found that excessive fibronectin interferes with communication between cells by activating abnormal signals through integrins, proteins that help cells sense and respond to their surroundings, and an enzyme known as focal adhesion kinase.

These abnormal signals disrupt a network of growth factors called VEGF, HBEGF, and IGF1. Although growth factors are often associated with cell development and repair, these particular signaling molecules also help astrocytes and blood vessel cells coordinate their activities to maintain a healthy blood-brain barrier.

When their communication becomes disrupted, the barrier can lose its integrity, potentially leaving brain tissue more vulnerable to damage.

“Single-cell analysis allowed us to examine this pathway in the different cells that maintain the brain’s blood vessels,” says co-first author Elanur Yilmaz, an associate research scientist in the Kizil lab. “We observed the same biological pattern across experimental models and human Alzheimer’s tissue, making the mechanism especially compelling.”

Evidence From Human Brains Strengthens the Alzheimer’s Connection

Importantly, the researchers found signs of similar biological disturbances in human samples, suggesting that the process identified in laboratory experiments may also contribute to Alzheimer’s disease in people carrying APOE ε4.

Analyses of brain tissue and cerebrospinal fluid showed that elevated fibronectin levels were associated with inflammation in astrocytes.

Genetic and gene-regulation analyses also connected FN1 to blood vessel disease and changes involving VEGFA, a growth factor that plays an important role in maintaining healthy brain blood vessels.

Together, these findings provide multiple lines of evidence linking excess fibronectin to the vascular damage associated with APOE ε4.

“The convergence of these independent human datasets strengthens the case that fibronectin is part of the APOE ε4-related vascular disease process,” says Badri Vardarajan, associate professor of neurological science in the Department of Neurology, Gertrude H. Sergievsky Center, and Taub Institute, who collaborated on this discovery of the FN1 mutation.

A Rare Genetic Defense Could Inspire New Alzheimer’s Treatments

The potential implications are significant because APOE ε4 is the strongest common genetic risk factor for Alzheimer’s disease. Approximately one in five people carries at least one copy of this gene variant.

Although carrying APOE ε4 does not guarantee that someone will develop Alzheimer’s, it increases their likelihood of developing the disease. Understanding why certain carriers remain unaffected could reveal new opportunities for prevention and treatment.

The latest findings suggest several possible approaches.

One strategy would be to prevent harmful amounts of fibronectin from accumulating around the brain’s blood vessels. Another would involve blocking the abnormal cellular signals triggered by excess fibronectin. A third possibility would be to restore the growth factor signaling that allows astrocytes and blood vessel cells to maintain the blood-brain barrier.

Researchers are already investigating these possibilities through laboratory experiments.

However, translating the discovery into a treatment will require considerable care. Fibronectin performs essential functions throughout the body, including supporting tissue structure and helping damaged tissues heal. Any future therapy would therefore need to target its harmful accumulation or effects without disrupting these beneficial activities.

By identifying the molecular mechanisms involved, scientists now have a more precise framework for designing such treatments. The findings may also help researchers determine when interventions would be most effective and how to measure whether they are successfully protecting the brain.

“By showing how fibronectin contributes to early vascular damage, this study gives us new therapeutic targets and potential ways to measure whether treatments are working,” says Richard Mayeux, chair of the Department of Neurology and a collaborator on the project. “Clinically, it connects a major genetic risk factor for Alzheimer’s to an early disease process that may be possible to modify.”

Although these potential therapies remain experimental, the discovery offers a promising new direction in Alzheimer’s research. Rather than focusing only on the damage that develops as the disease progresses, scientists may eventually be able to reproduce a natural genetic defense that helps protect vulnerable brains before significant damage occurs.

The researchers tracked almost 300 older adults with early brain signs of Alzheimer’s for nine to 11 years using pedometers. They found that physical activity didn’t reduce the toxic amyloid plaques that most Alzheimer’s treatments now target.

Instead, in people who already had these plaques, physical activity reduced the accumulation of misfolded tau proteins in specific brain areas. These proteins appear later in Alzheimer’s disease and are more closely linked to cognitive and functional decline. These signs of dementia were reduced by almost half in more active participants.

Benefits appeared at just 3,000 steps – roughly half an hour of walking at a moderate pace. The optimal range was 5,000 to 7,500 steps daily, after which the effect plateaued. More steps didn’t necessarily mean greater protection, which suggests a realistic target for older, sedentary people, rather than the often-cited 10,000 steps.

The study had limitations, however. It involved a fairly small group of mostly white, well-educated people in the US, and it didn’t take other lifestyle or health factors into account. Also, there may be other protective mechanisms of walking at play. But it does support other research suggesting that being physically active may lower the risk of dementia.

A UK study of 1,139 people over 50 found that those who were moderately to vigorously active had a 34-50% reduction in dementia risk when followed over eight to ten years. Among those who developed dementia, staying active reduced their memory decline, particularly in older women.

A larger 2022 UK study tracked 78,430 people for seven years using wrist accelerometers. It found a 25% reduction in dementia risk with just 3,800 steps daily, rising to 50% at 9,800 steps.

However, people who walked more also had better cardiovascular health – lower cholesterol, better sleep and blood pressure and reduced diabetes risk. Since these heart and stroke risk factors also increase dementia risk, the picture is complex.

Healthy habits often go together. People who exercise are more likely to eat well, not smoke, look after their heart health and have fewer financial stresses. This makes it hard to know which factor is having the biggest effect. The researchers tried to account for this, but because these habits are so closely linked, it’s difficult to say that exercise alone is responsible.

However, there is a strong case for this as there are multiple ways exercise might support the brain: improving cardiovascular health, increasing blood flow and boosting chemicals that promote brain-cell connections.

One such substance is irisin, a hormone produced by muscles that acts on almost all faulty brain mechanisms associated with Alzheimer’s, including inflammation. This and other chemicals, such as BDNF, associated with exercise, provide plausible biological pathways for how physical activity might directly influence brain health beyond its cardiovascular benefits.

But the relationship might work in reverse, too. People may become less active because of early Alzheimer’s symptoms. Those with hearing problems, for instance – itself a dementia risk factor – often report barriers that make them stop being active before other dementia symptoms appear.

Vicious circle

Reduced activity then accelerates memory decline. This creates a vicious circle. Early disease symptoms – such as not hearing – can affect self-esteem and reduce engagement in physical activity, which in turn worsens cognitive decline.

Brisk walking might be particularly beneficial. A small trial of 15 people with mild to moderate Alzheimer’s who did Nordic walking (an enhanced walking technique that uses poles to work your upper body as well as your legs) maintained brain function over 24 weeks, with some functions even improving.

The 15 who received only standard care showed decline or no improvement. Though small, the trial suggests that even people already diagnosed with Alzheimer’s might benefit from increased physical activity, including brisk walking.

Getting outside, particularly in nature, may be especially beneficial for preventing dementia – possibly because it improves mood and sleep while reducing isolation – all dementia risk factors. The combination of physical movement, natural light exposure and social interaction when walking outdoors may create multiple protective effects that complement each other.

The challenge now is helping people overcome barriers to outdoor activity, such as safety concerns, fear of falling, or simply preferring the comfort of the sofa – particularly during wetter, colder months. But the evidence suggests that even a few minutes of walking could make a difference, and that modest, achievable targets – a half-hour stroll rather than a marathon training regime – may offer substantial protection against cognitive decline.

In a study published in Physical Review Letters, researchers from the group led by Hanns-Christoph Nägerl, working with theoretical physicist Alvise Bastianello of the CNRS and Université Paris-Dauphine, describe how to engineer an exotic quantum state known as a “fractional Fermi sea.”

The breakthrough involves pushing ultracold cesium atoms far beyond their normal conditions by repeatedly changing how strongly they attract or repel one another. Rather than simply becoming disordered, the particles rearrange themselves into an unusual configuration that behaves differently from the quantum systems scientists have traditionally studied.

The theoretical findings provide the foundation for recent experimental research conducted by Nägerl’s team at the Department of Experimental Physics.

Pushing Quantum Particles Beyond Their Normal Limits

Under ordinary conditions, quantum particles follow well-established rules that determine how they arrange themselves, particularly at extremely low temperatures.

One important example involves fermions, a category of particles that includes electrons. These particles cannot all occupy the same quantum state, so they fill available energy levels according to specific restrictions. At very low temperatures, this arrangement produces what physicists call a Fermi sea.

But what happens when researchers deliberately disrupt the conditions that normally govern how particles behave?

As Alvise Bastianello explains: “Fermions, for instance, stack neatly into the available energy states to form the so-called ‘Fermi sea’. But what happens if one forces interacting atoms to continuously cycle through extreme conditions, smoothly shifting them from strongly repelling each other to strongly attracting each other?”

To investigate this possibility, the researchers studied ultracold cesium atoms confined to a one-dimensional system. This means the atoms are restricted to moving along a single direction, creating an environment in which their quantum interactions can be studied with exceptional control.

The team examined what happens when the interactions between these atoms are repeatedly adjusted, cycling between powerful repulsion and attraction.

Their calculations revealed something unexpected. Starting from the ground state, the lowest energy configuration available to the system, the atoms could be driven into a highly excited state without losing their underlying organization.

The researchers call this unusual arrangement a fractional Fermi sea because its particles appear to obey a modified rule governing how quantum states are occupied.

“Instead of simply heating the system, the interaction cycle reorganizes the atoms into a new many-body state,” says Yi Zeng, the leading author of this study. “This gives us a controlled way to explore quantum matter beyond the usual equilibrium paradigms.”

A Strange New Quantum State With Hidden Order

One of the most intriguing features of the fractional Fermi sea is that its particles remain organized even though the system has been pushed far from equilibrium.

In physics, equilibrium describes a condition in which a system’s overall properties have settled into a stable balance. Systems driven far from equilibrium can behave in complicated and unexpected ways, making them particularly challenging to understand.

Yet the fractional Fermi sea is not simply a collection of excited particles behaving randomly. Instead, it contains distinctive mathematical patterns that reveal a deeper structure.

Among these patterns are pronounced ripples called Friedel oscillations. These are wave-like variations associated with the way quantum particles influence one another. The researchers also identified unusual patterns in how correlations between particles weaken with increasing distance, even when the repulsive interactions are relatively weak.

These signatures are important because they differ from predictions associated with Tomonaga-Luttinger liquid theory, a long-established framework for describing how interacting quantum particles behave in one-dimensional systems.

The findings therefore point toward a previously unexplored type of quantum behavior that cannot be fully described using this familiar theoretical picture.

“This state is highly excited, but it is not random,” says Hanns-Christoph Nägerl, the group leader. “It has a hidden order that becomes visible in its correlations.”

The strange behavior also raises questions about the effective particles that emerge within the system. Physicists call these collective excitations quasiparticles because they can behave like individual particles even though they arise from the coordinated motion of many interacting particles.

Nägerl suggests that the unusual excitations might eventually deserve a name of their own.

“We are not yet sure how we should name these new quasiparticles. Perhaps ‘super-Fermions’?”

Opening a New Frontier in Quantum Physics

The discovery suggests that fractional Fermi seas represent an exotic critical phase of quantum matter, with characteristic patterns of particle correlations that extend beyond existing descriptions of one-dimensional quantum systems.

It also demonstrates the growing power of quantum simulation, a technique that allows scientists to use carefully controlled quantum systems to investigate physical behavior that would otherwise be difficult to reproduce or study.

Ultracold atoms are particularly useful for this purpose because researchers can precisely adjust their interactions and observe how the resulting quantum states change.

Rather than limiting these experiments to recreating phenomena already understood through established theories, scientists can now explore deliberately engineered states that reveal entirely new possibilities.

As Hanns-Christoph Nägerl says: “The discovery of fractional Fermi seas shows how far we can push quantum simulation: not only reproducing known models, but creating and probing states that go beyond established paradigms.”

The current publication establishes the theoretical framework for fractional Fermi seas. A companion study describing their experimental realization through quantum simulation is undergoing peer review.

Together, the research points toward new ways of investigating the fundamental behavior of quantum matter, including unusual collective excitations and hidden forms of order that emerge only when particles are pushed far outside their normal conditions.

To investigate this question, researchers in Canada examined the effects of psilocybin on the amphibious mangrove rivulus fish (Kryptolebias marmoratus). Their findings, published in Frontiers in Behavioral Neuroscience, suggest that even a brief exposure to a low dose can significantly reduce aggressive behavior without disrupting normal social interactions.

“We show that an acute, low dose of psilocybin significantly reduces activity and aggressive attack behavior during social interactions in adult mangrove rivulus fish, a species that is naturally highly aggressive,” said first author Dayna Forsyth, a research associate and former MSc student at Acadia University in Nova Scotia.

“These findings provide the first evidence that psilocybin can selectively reduce escalated aggression in a vertebrate model without suppressing social interaction,” added senior author Dr. Suzie Currie, a biologist at The University of British Columbia.

Why Scientists Studied Aggressive Mangrove Rivulus Fish

Mangrove rivulus fish are naturally combative, particularly when they encounter another member of their species. Their aggressive responses are easy to recognize and measure, allowing researchers to detect even small changes in behavior.

These fish also have an unusual reproductive ability. They can fertilize themselves, producing offspring that are genetically identical. This makes them especially useful for experiments because scientists can minimize genetic variation and more confidently attribute behavioral differences to psilocybin rather than inherited traits.

For the experiment, the researchers worked with three genetically distinct lines of fish bred in the laboratory. One group received psilocybin, another provided the fish used to provoke social interactions, and the third helped researchers measure how much psilocybin entered and accumulated in the animals’ bodies.

The researchers first established a baseline for each fish’s behavior. They placed a fish into a tank already occupied by another fish, with the two separated by a fiberglass mesh barrier and an opaque cover. The mesh prevented physical contact while allowing the fish to see and smell each other once the cover was removed.

After allowing five minutes for the fish to adjust to their shared environment, the team removed the opaque cover and recorded their interactions.

The following day, 24 hours after the initial observation, the researchers placed the same fish in water containing dissolved psilocybin. Following 20 minutes of exposure, they returned it to the tank with the same fish it had encountered previously. The opaque cover was then removed again so the researchers could observe any changes in behavior.

Magic Mushroom Compound Reduces Aggressive Attacks

The results revealed a striking change. Fish exposed to psilocybin moved around less and displayed fewer bursts of aggressive swimming than fish that had not received the substance.

To assess these changes, the scientists measured overall activity (time spent moving) and several signs of aggression (including swimming bursts). These rapid bursts are particularly important because they indicate that an encounter is escalating toward an attack, even when the fish cannot make physical contact.

“Swimming bursts are high-energy attack behaviors that represent an escalation of aggression towards the stimulus fish without making physical contact,” explained Currie. “Other types of aggressive behaviors, like head-on displays, are more about communication and social assessment and require very little energy.”

Interestingly, psilocybin did not suppress every form of aggressive or social behavior. While the fish became less likely to engage in intense, energy-demanding attacks, their less physically demanding social displays remained largely unchanged.

“Psilocybin’s calming effect appears to selectively reduce energetically costly, escalated behaviors while lower-energy social display behaviors remained largely unchanged,” said Forsyth. “This suggests that this compound can selectively dampen escalated social conflict rather than shutting down behavior altogether.”

The compound also reduced general activity. When placed alongside another member of their species, fish treated with psilocybin spent less time swimming than untreated controls.

Together, these findings suggest that psilocybin may influence specific aspects of aggressive behavior rather than simply making animals less responsive to their surroundings.

What the Findings Could Mean for Psychedelic Research

The researchers believe animal studies like this one could eventually help scientists better understand how psychedelic compounds influence behavior and identify possible directions for therapeutic research.

By examining which social responses are most sensitive to psilocybin, researchers may be able to uncover biological mechanisms that are difficult to investigate directly in people. Such insights could ultimately inform studies of potential clinical applications.

However, the team emphasized that the findings should not be interpreted as evidence of a treatment for aggression in humans. The experiment involved fish, did not evaluate any clinical intervention, and cannot establish whether similar effects would occur in people.

There are also important questions about how long the calming effect lasts. The researchers examined only single doses and short exposure periods. They did not investigate repeated treatments, long-term behavioral changes, or whether the fish might adapt to the substance over time.

Additional experiments will be necessary to determine whether psilocybin’s ability to reduce aggressive attacks can persist beyond the brief period examined in this study.

“Future studies can build on this work to explore how psilocybin alters neural signaling, which serotonin pathways are involved, and why some aspects of social behavior are affected while others are not,” concluded Currie. “These are questions that are difficult or impossible to answer directly in humans.”

Three physicists responsible for the breakthrough have been named recipients of the 2026 Europhysics Prize, one of Europe’s most prestigious honors in condensed matter physics. The European Physical Society (EPS) Condensed Matter Division selected Professor Jairo Sinova of Johannes Gutenberg University Mainz (JGU), Dr. Libor Šmejkal, and Professor Tomas Jungwirth for their work establishing altermagnetism as a distinct form of magnetic order alongside ferromagnetism and antiferromagnetism.

“This award recognizes a fundamental discovery that challenged one of the most established paradigms in condensed matter physics,” said Professor Jairo Sinova, Director of the Spin Phenomena Interdisciplinary Center (SPICE) at Mainz University. “Discovering that an entirely new magnetic phase had remained hidden for more than one hundred years demonstrates that even the most mature scientific fields can still hold fundamental surprises.”

The breakthrough emerged from years of collaboration between Sinova’s research group at Mainz University and Jungwirth’s team at the Institute of Physics of the Czech Academy of Sciences in Prague. Šmejkal, who also maintained an affiliation in Prague, spent eight years at Mainz between 2016 and 2024, first pursuing doctoral research and later working as a postdoctoral scientist in Sinova’s group.

During that period, Šmejkal played a leading role in developing the theoretical framework behind altermagnetism. By combining advanced mathematical approaches to symmetry with spintronics, which studies how electron spin can be used in electronic devices, the researchers identified a previously unrecognized pattern of magnetic behavior.

Their predictions soon attracted experimental teams around the world. Measurements of electronic properties and electrical transport in multiple materials provided evidence supporting the new magnetic classification. Altermagnetism has since grown into one of the most active areas of condensed matter physics, with research efforts expanding across Europe, North America, and Asia.

A Third Form of Magnetism Rewrites Physics

For more than 100 years, physicists generally divided collinear magnets into two fundamental categories: ferromagnets and antiferromagnets.

Ferromagnets have an overall magnetic alignment that produces a net magnetization. These materials are essential to many magnetic memory technologies used today. In conventional antiferromagnets, opposing magnetic moments cancel one another, leaving no overall magnetization and producing electronic behavior very different from that of ferromagnets.

Altermagnetism introduces a surprising third possibility.

Like antiferromagnets, altermagnets have magnetic moments that cancel out, resulting in no net magnetization. However, their electrons can exhibit properties previously associated with ferromagnets.

This unusual combination allows altermagnets to support electrical currents with strongly polarized electron spins while also displaying extremely rapid magnetic dynamics. Those characteristics could make them valuable for a new generation of spintronic devices, potentially advancing the speed and capabilities of future information technologies.

The significance extends well beyond electronics. Altermagnetism represents a previously unrecognized symmetry class of matter and has revealed unexpected connections to several major areas of modern physics, including topological phenomena, unconventional superconductivity, and quantum materials with strong interactions between electrons.

How Scientists Discovered Altermagnetism

The path toward this discovery began with theoretical investigations into unusual ways that electricity moves through magnetic materials. Among the early advances was the prediction of the crystal anomalous Hall effect, a phenomenon involving electrical transport in certain crystal structures.

Initially, these unexpected behaviors might have appeared to be unusual features of individual materials. However, the researchers eventually recognized that they were connected by a broader principle involving symmetries of electron spins.

Rather than representing isolated exceptions to established magnetic behavior, these materials belonged to an entirely different magnetic category.

A major milestone came in 2022, when the team published a comprehensive symmetry classification of altermagnetism and identified hundreds of materials that could potentially exhibit it.

Experimental physicists subsequently tested these predictions using several complementary methods. These included angle-resolved photoemission spectroscopy (ARPES), which reveals how electrons behave inside materials, along with measurements of electrical transport.

The results confirmed altermagnetic behavior in several materials, helping establish the new classification experimentally.

Interest in the discovery has expanded rapidly. Hundreds of scientific papers have appeared within just a few years, and altermagnetism has become a prominent subject at international physics conferences. The growing research community is now investigating both its fundamental properties and its potential technological applications.

Discovery Earns Prestigious 2026 Europhysics Prize

The Europhysics Prize recognizes major advances in condensed matter physics, a field concerned with the physical properties and behavior of materials. Established in 1975, the award honors discoveries that have significantly advanced scientific understanding, with a substantial share of the recognized research conducted in Europe.

The 2026 prize recognizes the theoretical and experimental advances that established altermagnetism as a new fundamental form of collinear magnetic order.

The award ceremony was scheduled for September 2026 at the 32nd General Conference of the European Physical Society Condensed Matter Division (CMD32) in Graz, Austria.

The Scientists Behind the Breakthrough

Professor Jairo Sinova is a physics professor at Johannes Gutenberg University Mainz in Germany and director of the university’s Spin Phenomena Interdisciplinary Center. His research investigates magnetism, spintronics, and quantum materials.

Dr. Libor Šmejkal conducted much of the crucial theoretical work that led to the identification of altermagnetism while working at Mainz University from 2016 to 2024. His current affiliations include the Max Planck Institute for the Physics of Complex Systems, the Max Planck Institute for Chemical Physics of Solids, and the Institute of Physics of the Czech Academy of Sciences.

Professor Tomas Jungwirth is affiliated with the Institute of Physics of the Czech Academy of Sciences and the University of Nottingham. He has collaborated extensively with Sinova’s Mainz research team and played a central role in establishing the theoretical foundations of altermagnetism.

Together, their work has revealed a fundamental property of magnetic matter that escaped recognition for more than a century, opening an entirely new direction for research into quantum physics and future electronic technologies.