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I was fifteen when I first read Oliver Sacks. His accounts of the brain, and of the people living with its disorders, made me want to understand the organ that produces the mind. I studied medicine and a research master's in neuroscience, and from early on my interest settled on schizophrenia, one of the most fascinating and least understood conditions in medicine.

I now work as a psychiatrist with patients who have treatment-resistant schizophrenia, meaning the usual medications have not helped them enough. Seeing them every week sharpens one question: after decades of research aimed almost entirely at neurons, why do our treatments still do so little for so many people? I work on neurons too. But I have always been drawn to questions others tend to skip, and that curiosity has grown into three lines of research. In March 2026 the Schizophrenia International Research Society gave all three an Early Career Award in Florence.

The first line grew out of my fascination with the brain's blood vessels, which began during my PhD on how blood vessels form in brain tumours. The blood-brain barrier (BBB), the specialised structure separating blood from brain, matters in schizophrenia for a simple reason: the brain runs almost entirely on glucose from the blood, and nearly all of it has to cross this barrier first. Together with Dr Dana Mustafa, who co-supervised my doctorate, and her team at Erasmus, we studied the barrier in postmortem brain tissue from the Netherlands Brain Bank, using spatial transcriptomics, a method from cancer research that measures the activity of thousands of genes while recording exactly where in the tissue each measurement was taken. We focused on the insular cortex, a region involved in schizophrenia but rarely studied in this detail, and looked separately at the BBB and the brain parenchyma beside it. The two normally run on different energy systems, the BBB mainly on glycolysis and neurons mainly on mitochondrial metabolism. In schizophrenia both appeared to be working harder than in people without the illness. That was unexpected, because most earlier research carried out in the prefrontal cortex had found brain metabolism turned down in schizophrenia. Seeing it turned up in the insula suggests these changes may differ from one region to another rather than being the same throughout the brain. This is an early, proof-of-concept study in a small number of donors and needs confirmation in larger ones.

The second line is older than it looks. In 2005, as a neuroscience student, I proposed testing a ketogenic diet for schizophrenia. It was not funded and I let it go. Years later I returned to it, and the rejected proposal is now a research programme I lead, with more than 800,000 euros in funding over three years, one trial finished and two larger ones in preparation. The restrictive ketogenic diet that helps in some forms of epilepsy can be extra challenging for patients with severe illness to maintain, so we use a drink containing ketones instead. It raises blood levels of ketone bodies, which give the brain an alternative fuel and also act as signalling molecules with various downstream effects. If the brain's energy supply is part of the problem in schizophrenia, this is one way to work on it.

The third line steps outside the brain. Some of the body's most informative signals, such as the stress hormone cortisol or the sleep hormone melatonin, rise and fall throughout the day, so a single blood sample tells you little. With a group at the University of Texas at Dallas, we are testing a wearable sweat sensor, about the size of a watch, that measures several of these markers every few minutes, day and night. Continuous readings like these could help us follow signals such as stress and the sleep-wake rhythm far more reliably than we can today, across many psychiatric conditions including schizophrenia.

None of this is solo work. Each line depends on a team. I owe a great deal to my mentor Dr Nico van Beveren, who backed these unconventional directions and helped turn them into real studies, and to Dr Dana Mustafa for her rigorous scientific teaching, enthusiasm and support. SIRS has been valuable in a different way: the Congress brings clinicians, scientists, patients and families together, and the award connected me to people who take unusual questions seriously.

Better care for people with schizophrenia is urgently needed. I hope that twenty years from now, we can say we achieved it.

Karin Huizer, MD, PhD, is a psychiatrist at Antes (Parnassia Groep), the Netherlands, and a 2026 SIRS Early Career Awardee.

By Camila M Loureiro, MD, PhD, Assistant Professor at the School of Nursing, University of São Paulo (Brazil), SIRS Early Career Awardee 2026

I have always been fascinated by understanding how biology and life experiences come together to influence the development of psychosis. Throughout my career in neuroscience and psychiatry research, I became particularly interested in this field because psychosis often begins during adolescence or early adulthood, a time when young people are building their futures, relationships and sense of identity. Its impact can be profound, affecting not only individuals but also their families. Despite decades of research, many important questions remain unanswered, particularly how environmental and biological factors interact and how we can identify people at risk before symptoms become severe. These questions continue to drive my research today.

My work focuses on epigenetics, a field that explores how environmental exposures can influence gene function without changing the DNA sequence itself. I am particularly interested in understanding how environmental risk factors become biologically embedded during the early stages of psychosis and why some individuals are more vulnerable than others. Ultimately, I hope this research will contribute to earlier identification and more personalised approaches to preventing and treating psychosis.

At the 2026 SIRS Congress, I presented findings from a study investigating changes in a gene involved in the brain’s endocannabinoid system, which helps regulate functions such as memory, learning and emotions. Because cannabis acts on this system, we wanted to understand whether these biological changes were related to psychosis itself or to cannabis use. We found that people with early psychosis showed differences in the regulation of this gene regardless of cannabis exposure, suggesting that some biological changes may be linked to psychosis independently of cannabis use. These findings are important because they remind us that psychosis is not caused by a single factor. Rather, it emerges from a complex interplay between genetic vulnerability, environmental exposures, brain development and biological adaptations that we are only beginning to understand. Our results also highlight an important lesson for psychiatric research: biological signatures associated with environmental exposures do not always mirror those associated with disease states.

Receiving a SIRS Early Career Award was an important milestone in my professional development. Attending the Congress gave me the opportunity to present my research to an international audience, discuss my findings with experts from around the world and establish new scientific connections. One of the most valuable aspects of the experience was participating in the mentorship programme. I was fortunate to be mentored by Professor Graham Murray from the University of Cambridge. Our discussions about research direction, career development and future opportunities encouraged me to think more broadly about how my work can contribute to the field of early psychosis research. The experience reinforced the importance of collaboration and the value of learning from researchers with different perspectives and expertise.

Currently, I am an Assistant Professor at the School of Nursing, University of São Paulo (USP), Brazil, where I investigate how environmental risk factors, epigenetic mechanisms and other biological processes interact during the early stages of psychosis. My research integrates different disciplines to better understand the pathways underlying psychosis and support the development of earlier, more holistic and targeted interventions. As a nurse researcher, I am particularly interested in translating scientific discoveries into preventive strategies and improving the delivery of care for people at risk of psychosis. As a researcher based in Brazil, I am committed to generating evidence that reflects the diversity of populations often underrepresented in psychiatric research, helping to ensure that future advances in psychosis prevention and care can benefit people across different social and cultural contexts.

When I think about a young person developing psychosis 20 years from now, I hope they will benefit from a more tailored, preventive and equitable approach to care. Instead of relying solely on symptoms to guide treatment decisions, clinicians may be able to integrate biological, environmental and social information to identify risk earlier and provide timely and individualised support before the illness significantly disrupts a person's life. Ultimately, my hope is that research will not only advance our understanding of psychosis but also help people preserve their daily lives, relationships, education and future opportunities. Although there is still much work to be done, I am optimistic that, through collaboration, innovation and support from organisations such as SIRS, we can meaningfully improve the lives of people affected by psychosis and their families.

Soyolsaikhan Odkhuu, Ph.D. — Research Assistant Professor, Department of Psychiatry, Jeonbuk National University Medical School, Republic of Korea

I did not begin in medicine. I trained as a physicist. As an undergraduate in Mongolia, I studied not only physics but also electronics, building and analysing analogue circuits and learning to solve a problem by taking a system apart to see how its pieces fit together. Later, during a master's degree, I worked on the computational side of physics. What eventually drew me toward psychosis research was, in a way, a physicist's question. The brain is the most intricate network we know of, and I became fascinated by what happens to that network when a person's sense of reality begins to change. The field, I found, was full of questions that had barely been explored. I did not want to chase techniques for their own sake; I wanted to use them to understand the brain and mental health. Moving from physics into psychiatry let me bring the mathematics of networks to one of the hardest problems in medicine.

And it is a hard problem, partly because schizophrenia is not a single thing. Two people with the same diagnosis can follow very different paths — different symptoms, different responses to treatment, different chances of recovery. To me, one of the most important questions in our field is whether we can find biological signs that capture those differences: markers that tell us not only that someone has psychosis, but what kind, how far it has progressed, and what is likely to come next. Today we still rely mostly on interviews and observed symptoms. We do not yet have that biological map.

My research tries to build part of it by studying the brain as a network. Picture a transport map: brain regions are the stations, the connections between them are the routes, and a handful of major hubs hold the whole system together. Using scans taken while a person is simply resting, I measure how resilient that network is — and to do this, my colleagues and I "stress-test" it on a computer, removing the busiest hubs one at a time and watching how quickly the rest of the map falls apart. A resilient network reroutes gracefully; a fragile one comes apart early.

Across several studies, a consistent picture has emerged. In people experiencing their first episode of a schizophrenia-spectrum disorder, these core networks were measurably less resilient than in healthy individuals — and the people whose networks held up best also tended to have sharper thinking and milder symptoms. In another study, I looked at people who had recovered well enough to stop their medication; those whose networks were less resilient were more likely to relapse afterward, while those with sturdier networks tended to stay well. And when I compared schizophrenia with a milder, harder-to-classify form of psychosis, that second group sat in between — their networks partly preserved, as if reflecting a genuinely different biology rather than simply a milder version of the same illness.

Why does this matter outside the laboratory? Because a measure of network resilience could eventually help with real decisions. It might help a clinician weigh who can safely come off medication and who needs closer follow-up. It might flag, early on, who is most vulnerable, so that support arrives sooner rather than later. Imagine a young person who develops psychosis twenty years from now: the hope behind this work is that, instead of a long stretch of trial and error, their care could be guided by a read-out of how their brain is actually coping — personalized from the very start.

This past year I had the privilege of presenting some of this work at the SIRS Annual Congress in Florence as an Early Career Awardee. While I presented, many researchers took an interest and asked me question after question — a fantastic and motivating experience for a young researcher, and one that sent me home with new ideas. What I value most about SIRS is that it brings together people from every corner of the world who are circling the same difficult questions, and it makes it possible for someone early in their career to be part of that conversation.

I am now leading a project to turn these resilience measures into a practical toolbox — one that can sort psychosis into clearer subtypes and stages of illness. If it succeeds, the goal is that when a patient first comes to the clinic, we could identify which subtype they have and how far the illness has progressed and begin to anticipate what lies ahead. My hope is that the brain's quiet ability to stay standing under strain — its resilience — turns out to be something we can measure, protect, and one day help to strengthen.

Looking through the eye to understand the brain

What first drew me to psychotic research was a deceptively simple frustration: we cannot see what is wrong. Unlike a broken bone on an X-ray or a tumor on a scan, the changes in the brain that underlie psychosis are largely invisible to us in living humans. Brain scans exist, of course, but they are expensive, demanding, and often distressing for patients who are already struggling. When a person experiences their first episode of psychosis, clinicians are largely working blind. They lack reliable biological markers to guide them on who is at highest risk, when to intervene, or how well a treatment is working.

The eye as a window to the brain

So we and others started asking a different question. What if we didn't have to look at the brain directly? The retina, which is this thin layer at the back of your eye that captures light, is actually a direct extension of the brain. Developmentally, it grows from the same tissue. It shares the same cell types, the same molecular machinery, and many of the same vulnerabilities. And critically, we can image it in a few minutes with a device called an optical coherence tomography (OCT) scanner, at a very competitive cost. And this cool thing is this device can be found in many eye clinics and hospitals already.

My research over the past several years, conducted at the Psychiatric University Hospital Zurich with Prof. Philipp Homan and a talented group of international collaborators, has focused on one central question: can the retina tell us something about a person's risk for schizophrenia, before symptoms even appear?

The answer is yes, and go deeper than we expected. In two studies published in Nature Mental Health and JAMA Psychiatry, my colleagues and I examined data from over 36,000 people in the UK Biobank — a large health research database of people without a schizophrenia diagnosis. We looked at their genetic risk for schizophrenia (calculated from their DNA) and compared it to the microscopic thickness of their retinal layers. People with higher genetic risk for schizophrenia had subtly but measurably thinner retinas — specifically in a layer called the ganglion cell inner plexiform layer. This layer contains the synaptic connections of a type of retinal cell called amacrine cells - interneurons that process signals within the eye. Crucially, these same cells turned out to harbor a striking concentration of schizophrenia risk genes, and this finding held up across humans, monkeys, and mice, and even in fetal retinal tissue, suggesting it traces back to early brain development.

In other words: the genetic "signature" of schizophrenia is written not just in the brain, but probably also in the eye, specifically in cells whose job involves synaptic communication. This provides some of the further evidence that schizophrenia might be a disease of the synapse (i.e. the connection point between brain cells), and that this disruption begins long before a person ever experiences a psychotic episode.

Why this matters for patients and families?

Imagine someone showing some early warning signs that worry their family, friends or partners. Early intervention is known to dramatically improve outcomes. This means a shorter period of untreated psychosis means better cognitive functioning, better social integration, more autonomy again. But today, identifying who among those at-risk individuals will actually go on to develop psychosis is still very difficult. We believe, we - together with others - laid the foundations with our retina research for future studies that will test how informative retinal changes are for early detection, risk stratification and treatment monitoring. If fruitful, a simple eye scan at the first appointment together with some questions by the psychiatrist could be all to determine someone’s brain health.