Psychiatry Research Trust
2026 Alfred Meyer Prize Winners
The Alfred Meyer Prize is awarded for outstanding research on the relationship between brain mechanisms and mental illness. We are delighted to announce the 2026 inaugural prize winners, Martin Osugo and Luke Vano. Explore their winning publications below.
Martin Osugo
Striatal dopamine D2/D3 receptor regulation of human reward processing and behaviour
A longstanding challenge in psychiatry has been to show clearly how changes in brain chemistry lead to the symptoms that define major mental illnesses. Disability in diseases like schizophrenia and Parkinson’s disease are often due to symptoms such as reduced motivation for activities, reduced experience of pleasure, and reduced emotional expression. These symptoms are collectively termed negative symptoms, and are thought to arise from abnormalities in the brain’s reward system linked to changes in the neurotransmitter dopamine.
This view is based on decades of research in animals, and indirect tests of dopamine function in humans. However, there has been no direct evidence in humans showing that changes in dopamine function cause these symptoms. This is a critical gap in our knowledge, as disorders associated with negative symptoms affect around 200 million people worldwide.
To address this, we designed a study to test cause and effect directly. We compared two drugs which change dopamine signalling in the brain to a placebo (sugar pills), and neither the volunteers nor the researchers knew who was randomly chosen for each treatment (double-blind). We chose to carry out our study in healthy volunteers, because the two drugs we used are treatments for schizophrenia in clinical practice (antipsychotics). This means that if we ran the study in patients, it would be difficult to tell how much of any change in motivation and reward was because of the illness improving after treatment. Studying healthy volunteers meant that we could be confident that any changes in reward and negative symptoms were because of changes in dopamine after taking the drug.
Our main finding was that healthy volunteers who received amisulpride (a dopamine blocking antipsychotic) for 7 days at a dose used to treat schizophrenia developed negative symptoms. We also found a mechanism in the brain that may explain this, showing that amisulpride reduced the activation of an important part of the brain’s reward centre (the caudate) during a brain scanning task where volunteers could win money whilst in the scanner. Importantly, these two things were related to each other – so people who had more severe negative symptoms after receiving amisulpride also had greater reduction in their brain’s reward response to winning money.
We showed that this was not a general effect of all antipsychotics; we found that another antipsychotic, aripiprazole, did not have these effects in healthy volunteers who also received it for 7 days. We included this experiment with aripiprazole because amisulpride blocks dopamine receptors to a greater extent than aripiprazole. Aripiprazole is a more flexible drug which acts in a similar way to amisulpride when dopamine levels are high, but can also have the opposite effect when dopamine levels are low. This can be thought of as a bit like the difference between a dimmer switch (aripiprazole) and a standard light switch (amisulpride). Both drugs caused movement problems similar to those seen in Parkinson’s, but these were not related to changes in reward processing.
These findings provide the first direct evidence in humans that dopamine signalling regulates reward processing and motivated behaviour. They also show that the effects of dopamine on reward and motivation can be separated from its effects on movement, indicating that these functions are supported by different brain mechanisms.
Our findings have important implications for the tens of millions of people worldwide who take long-term antipsychotic treatment, and the clinicians who treat them. We show that these widely used treatments may worsen motivational symptoms by impairing reward processing. Many people with schizophrenia and other disorders associated with abnormalities in dopamine also experience negative symptoms even without any treatment, and this work improves understanding of how changes in dopamine may cause these symptoms. This may help guide the development of more effective treatments in future.
Luke Vano
The role of low subcortical iron, white matter myelin, and oligodendrocytes in schizophrenia
The brain requires many nutrients to function. One of the most important is iron. Iron’s high reactivity means it is essential for the production of key brain chemicals, such as dopamine and serotonin. However, if iron levels get too high, this reactivity can lead to brain damage, as seen in conditions such as dementia and Parkinson’s disease. This means that brain iron levels are kept in a delicate balance. Researchers have wondered whether altered brain iron levels contribute to schizophrenia, given that abnormalities of the dopamine and serotonin systems are associated with the condition.
Magnetic resonance imaging (MRI) produces images of the brain using magnets. As iron is highly magnetic, specific MRI sequences can be used to estimate brain iron levels. The use of this technique in schizophrenia has shown conflicting results, with some studies linking schizophrenia with higher brain iron levels and others with lower levels. This may be due to differences in myelin, which influences these MRI estimates. Myelin is a fatty coating that insulates nerve fibres and speeds up brain signalling. Lower levels of myelin in schizophrenia have been suggested to underlie abnormal brain activity.
To determine whether iron or myelin alterations are present in schizophrenia, we used an iron-sensitive MRI technique, which can be affected by myelin, alongside an MRI technique to measure myelin levels in 85 patients with schizophrenia and 86 matched healthy controls. We created a brain map showing where iron levels were most different in people with schizophrenia. This map was compared to a database of the concentration of different brain cells across brain regions. Through this comparison, we could estimate which type of brain cell was losing the most iron.
We found that the iron-sensitive MRI values were lower in patients with schizophrenia than in healthy controls. This decrease was largest in regions of the dopamine system (the caudate nucleus, putamen, globus pallidus, substantia nigra and ventral tegmental area). This finding could be due to a loss of iron or a gain of myelin in these regions. However, our myelin-sensitive MRI results linked schizophrenia to lower myelin levels. This indicates that both iron and myelin are lost in schizophrenia. Comparison of our map showing where iron loss was greatest with the map of cell concentration revealed that iron loss was greatest in regions rich in oligodendrocytes. Oligodendrocytes have the highest iron concentrations of all brain cells and produce myelin.
Taken together, our findings link schizophrenia to loss of both iron and myelin, alongside oligodendrocyte dysfunction. We propose a model in which iron deficiency in oligodendrocytes impairs myelin synthesis. Given that iron deficiency affects over 1 billion people worldwide, this may be a common, treatable risk factor for schizophrenia. Our findings also suggest that these MRI measures may be used for earlier detection of schizophrenia and to monitor disease progression.
