Meet our Cross-Hub Research Fellow Fabiana

Dr Fabiana Corsi-Zuelli investigates how immune and metabolic mechanisms interact with social and environmental factors to shape psychosis risk, symptom dimensions, and physical health outcomes. 

Fabiana is one of the recipients of the MHP Early Career Researcher Fellowship Awards, which aim to help develop future leaders in SMI research. Her project will bring together ImmunoMIND, Metabolic Psychiatry and Social Health Hubs. It’s called “Precision Immune-Metabolic Approaches in Psychosis: Bridging Genes and Immune Cells with Physical and Social Determinants of Health”. ​She tells us more about what this means.

Linking mental and physical health

For a long time, it was suggested that the immune system was simply overactive in psychosis. This was reflected by increased levels of circulating inflammatory proteins (“low-grade inflammation”) in people with psychosis. But, results from clinical trials testing antipsychotics in combination with broad anti-inflammatory drugs showed the addition of these drugs did not benefit symptoms.

My research asks whether cell-specific immune dysregulation could be one of the pathways which links mental and physical health. I will study changes in the immune system to see if they contribute to symptoms of psychosis and poor physical health. I will also investigate the relationship between immune dysfunction and social factors such as environmental stressors. 

This matters because psychosis is not only a brain disorder. Many people with psychosis also experience serious physical health problems, including type 2 diabetes, high cholesterol and cardiovascular disease.

What motivates me is the possibility of translating these mechanistic questions into more precise approaches to care. If we can use the immune system to identify subgroups or mechanisms, we may eventually be able to design better experimental medicine studies and more targeted interventions.

To address this, I use two complementary approaches. 

First, I analyse large genetic datasets using causal inference methods to test whether immune-cell changes are likely to have causal effects on psychosis, symptoms and cardiometabolic outcomes while accounting for social factors. 

Second, I analyse clinical cohorts of people in the early stages of psychosis, where we have detailed information on blood immune cells, symptoms, brain and body health, and adverse life experiences.

The long-term aim is to move from broad inflammatory markers towards more precise, cell-specific mechanisms that could eventually guide prevention, stratification and new treatment approaches.

Innovating through collaboration

No single method can answer the questions I am interested in. So, I collaborate with people who bring very different forms of expertise, and I think this is essential for a field like immunopsychiatry. 

Framing the science with PWLE

Patient and Public Involvement and Engagement (PPIE) is central to my work. My project was co-developed with people with lived experience and their input helped shape the focus on anhedonia, the reduced pleasure in psychosis. It reminded me that biological mechanisms need to be understood alongside personal experiences and environmental factors. 

I would recommend building PPIE into the research from the beginning, not only at the dissemination stage. It changed the way I framed the science.

I will continue this work through meetings, accessible updates and co-produced visual materials to make complex science meaningful and useful beyond academia.

Diversity is essential 

Through my involvement in the Latin America Genomics Consortium and PNIRS Ibero-America, I am committed to strengthening representation of Latin American and other underrepresented populations in immunopsychiatry and psychiatric genomics. These areas remain strongly shaped by European and North American datasets, which limits generalisability and risks leaving important biology underexplored. 

This is not only an equity issue; it is also essential for better science. More diverse cohorts can help us understand which findings are broadly generalisable and which are shaped by ancestry, environment, health systems and social context. My ongoing international collaborations are part of this effort to broaden immunopsychiatry beyond a narrow set of populations.

However, I think it is important to be cautious: this work is not about claiming that one immune cell or one drug will explain psychosis. Rather, it is about building a rigorous framework to identify which immune mechanisms matter, in whom, and under what conditions. 

I hope this work will contribute to a shift in psychiatry from symptom-based categories alone towards biologically informed mechanisms that can be tested, replicated and eventually translated into better care.