SIRS Research Stories

Yanhui Li, B.Sc., M.D.
Psychiatry Resident
Institute of Mental Health, Singapore

I am a Psychiatry resident at the Institute of Mental Health in Singapore and my work focuses on investigating immunological changes in schizophrenia and treatment resistance. We have recently performed one of the most ambitious and comprehensive immunophenotyping study on schizophrenia patients and healthy individuals, and identified immune cells significantly different between them. We specifically identified an immune cell ratio (the CD4/CD8 T cell ratio) as a potential biomarker for schizophrenia and treatment resistance. One of the most significantly altered populations included a special subpopulation of immune T cells found in the gut known as Mucosal-associated Invariant T (MAIT) cells. This is an exciting finding as MAIT cells are implicated in the gut-brain axis and autoimmunity, processes hypothesized to contribute to the pathophysiology of schizophrenia.

The immune hypothesis proposes that aberrant immunological mechanisms underlie the pathophysiology of schizophrenia. It has been controversial but has been one of the longest-standing ideas behind the etiology of schizophrenia, if we consider it to encompass infectious hypotheses since the early 1800s with the rise of bacteriology. Such ideas were further piqued with observations of “General Paresis of the insane” in neurosyphilis, and with the emergence of psychotic symptoms in encephalitis lethargica noted after the Great Influenza Epidemic in 1918. Today, there is growing evidence of immune involvement with genetic, proteomic, cellular studies, and even with neuroimaging and clinical trials with anti-inflammatory medications. The recent discovery of NMDA encephalitis in 2007 triggered a sharp spike in interest in the immune hypothesis of schizophrenia. Researchers began to question if a portion of schizophrenia patients may have subthreshold autoimmune processes driving psychiatric symptoms. Other mechanisms involving T cells and microglia (“cleaner” cells in the brain) have also been proposed.

Although the exact mechanisms of immune involvement in schizophrenia remain unclear, evidence strongly suggests immunological changes in a subset of patients, who also appear to benefit from anti-inflammatory agents. If we could identify this group and intervene with anti-inflammatory agents or target immunological processes, this may prove to be a new treatment modality or augment current available treatments. Up to a third of schizophrenia patients do not respond well to available antipsychotics and are prescribed clozapine, the gold standard medication in treatment-resistant schizophrenia. Among this group, there is a sizable number of ultra-treatment-resistant patients who are refractory to clozapine as well. Some patients are also refractory even with neurostimulation involving electroconvulsive therapy. Hence, a novel treatment modality is always welcome in broadening choices of available therapeutic options. Our study supports immune changes in schizophrenia, and we push the immune hypothesis further by showing apparent proportionate changes in immune cells with increasing treatment resistance. This adds to further evidence supporting immune involvement and the exploration of immune-targeted therapies moving forward.

I presented findings from our immunotyping study at the 2024 SIRS Annual Congress in Florence, Italy, and was fortunate enough to receive the Early Career Academic Excellence Award. This award comprised a mentoring component, and afforded me the opportunity to meet Dr Neeltje van Haren from Erasmus MC-Sophia Children’s Hospital. It was a pleasure to meet Dr Neeltje and her postdoc Lisanne, and I learnt much about their work in neuroimaging and the maternal-fetal interface. I appreciated the special reception for early career awardees as well, as it allowed me to meet peers from all over the world equally passionate about schizophrenia research in their individual domains. As what Dr Iris Sommer alluded to in her recent pre-election manifesto, I think SIRS is valuable in promoting the sense of community and inspiration among colleagues worldwide, as we work toward alleviating a common affliction of humankind, beyond the factual sharing and dissemination of scientific knowledge. This platform, beyond sparking scientific collaborations, appeals to the basic human need for community and support, and what better way to do this than on an international scale? With ongoing efforts at increasing diversity and representation of participants from all parts of the world, SIRS is well on its mission to becoming a worldwide organization aggregating clinicians and researchers working on schizophrenia-spectrum disorders. I highly recommend anyone working in schizophrenia-related research to attend a SIRS Congress, to see for yourself the superior quality of research and strong sense of community not frequently found in other conferences. I aspire to a career as a clinician-scientist after completing residency training, and I hope to remain actively involved in SIRS as long as I continue working with patients affected by the illness, and as long as I continue my work in this area.

I first became interested in psychosis spectrum disorders during the first year of my PhD at University College London. I had read about the work of Dr Rick Adams, who was using computational tools to study schizophrenia, and decided to pursue a rotation project with him. During the rotation, I learnt that we can investigate brain function without the need for invasive procedures by using mathematical models. This is crucial for two key reasons. First, it allows us to study psychosis directly in patients, accounting for important factors that cannot be fully captured in animal models. Second, it is more directly applicable to clinical practice, and could contribute to the development of new interventions.

As I delved into psychosis research, I also had to navigate the difficult experience of watching a loved one struggle with this condition. I became acutely aware of the stigma faced by those affected by psychosis, the difficulties associated with finding the right treatment, and the lack of guidance available for patients and their families. Indeed, despite the progress we have made over the past few decades in improving the understanding and treatment of psychosis, many important questions remain. What biological changes underlie the onset and progression of psychosis? How can we intervene earlier to improve outcomes? Can we develop more effective treatments with fewer side effects?

My research tries to tackle these questions by investigating biological changes in the early stages of psychosis. Specifically, I study the balance between excitatory and inhibitory activity in the brain – essentially, how different brain cells communicate to enable signal transmission whilst maintaining stability. This balance is crucial for brain function. It is altered, for example, in epilepsy, and it is also thought to become disrupted in psychosis spectrum disorders. My work focuses on individuals who are at a higher risk of developing psychosis, either due to a genetic predisposition or to experiencing symptoms, like unexplained sensory perceptions or odd thoughts, which do not meet the severity or frequency criteria for a psychosis spectrum disorder but are linked to higher conversion rates. Studying these early changes is important because it can help us understand how psychosis develops. It may also make it possible for doctors to tailor treatments for at-risk individuals before symptoms become severe.

At the SIRS 2024 congress, I presented results from my PhD research showing that both excitatory and inhibitory activity become altered in emerging psychosis. Using computational models and EEG, which measures electrical activity in the brain via small sensors placed on the scalp, I found evidence that changes affecting excitatory cells could be a primary cause of the illness. My findings also showed that reduced inhibition in the brain may contribute to the severity of symptoms. This is promising because it suggests that we could target these alterations using glutamatergic treatments. These treatments are not currently available for schizophrenia, but they have shown encouraging results in preclinical studies and have the potential to improve negative and cognitive symptoms – such as lack of motivation and difficulties with memory and attention – which are not addressed by current dopaminergic medications.

While there is still much to learn, this represents a first step toward more effective early interventions. Indeed, ongoing research is needed – for instance, to validate and improve the models that we use – but I am hopeful that we can make a meaningful impact by continuing to research excitation and inhibition in at-risk individuals. Attending the SIRS conference as an Early Career Awardee provided me with opportunities to learn about other advances and to receive feedback that inspired new research directions. Looking to the future, our goal is to explore how early interventions can be tailored based on individual brain function, and to study how brain changes relate to the development of specific symptoms. I believe that incorporating artificial intelligence into this research holds great promise for improving our understanding and enhancing treatment outcomes.

Recently, my loved one found a treatment that works for him, and has published a book sharing his experiences to raise awareness and inspire others facing similar challenges. I submitted my PhD thesis, and am looking forward to continuing investigating mental health as a postdoctoral researcher. I am confident that, with continued research and collaboration, we can achieve a better understanding of psychosis and offer hope to those affected by this condition.

I have always been captivated by understanding how the brain develops and how certain factors, such as genetics and life experiences, can shape a person’s vulnerability to mental health disorders such as schizophrenia. During my PhD studies under the supervision of Prof. Dr. Timothea Toulopoulou, I had the opportunity to work with both patients and healthy individuals, focusing on understanding the brain mechanisms involved in psychosis. Specifically, I am interested in how genetic and environmental factors like childhood trauma shape brain function. Psychosis, especially schizophrenia, is a complex disorder that affects how people think, feel, and behave. One way it impacts the brain is through changes in connectivity between different regions, particularly those involved in working memory—the ability to hold and manipulate information over short periods of time. By combining functional magnetic resonance imaging (fMRI) with twin data, I aim to better understand how brain connectivity is altered in people at risk for developing schizophrenia and how environmental and genetic factors affect these mechanisms. This research is important because it helps us understand not only the disruptions in the brain but also how some individuals seem to be more resilient to the effects of environmental stressors like trauma.

At the 2024 SIRS conference, I had the honor of receiving the Early Career Award, which provided a unique opportunity to present the findings of my latest study on the genetic resilience for schizophrenia and environmental risk on brain connectivity of adolescent twins. Schizophrenia is characterized by disruptions in the functional integration of working memory brain networks. Exposure to environmental risks during critical periods of brain development can disrupt the typical trajectory of brain maturation and increase the risk of schizophrenia. Investigating how genetic resilience, defined as a heritable measure of variation that increases resistance to disease by reducing the impact of risk loci, influences this link is critical to understanding the disorder’s causal mechanisms. To this aim, we collected fMRI data from 350 healthy twins oversampled for familiar schizophrenia risk. Functional connectivity indexes were calculated for each participant. We examined whether connectivity patterns in areas such as the paracingulate gyrus (PCG) and precentral area were predicted by environmental risks and how the polygenic resilience score for schizophrenia moderated this relationship. We found that genetic resilience moderated the relationship between environmental risk (discrimination and childhood trauma) and functional connectivity. For example, in individuals with lower levels of genetic resilience, childhood trauma reduced connectivity in the precentral region of the brain. Similarly, individuals who had lower levels of genetic risk discrimination decreased connectivity in the PCG. Individuals with higher genetic resilience did not show decreased connectivity in the same regions. Our findings underscore the interplay between genetics, environmental risk, and the neural mechanism in building resilience to schizophrenia. As PCG and precentral are relevant in schizophrenia, optimal connectivity in these regions may enhance a person’s ability to cope with adversity. The moderating role of genetic resilience highlights the importance of gene-environment interactions in investigating neural mechanisms responsible for genetic resilience to adversity.

Attending the SIRS conference as a young researcher was an invaluable opportunity. Not only was I able to share my findings with experts in the field, but I also had the opportunity to connect with researchers from all over the world. The chance to engage in discussions with other scientists and receive feedback on my research has been an invaluable experience.

Currently, I am in the final semester of my PhD and looking forward to continuing my research in the field of psychosis as a postdoc. I am passionate about continuing to work on how genetic and environmental risk factors shape brain development and may promote vulnerability to psychotic diseases by implicating brain mechanisms. Ultimately, my goal is to deepen the understanding of the neurobiological underpinnings of psychotic disorders to help develop early intervention strategies.

Treatment resistance in schizophrenia is a major clinical problem with one third of schizophrenia patients showing non-response to standard antipsychotic treatment. The delay in identifying these patients leads to prolonged ineffective treatment, longer hospitalization, unnecessary side effects and lower quality of life for those individuals. There is an urgent need for (bio)markers that can identify treatment-resistant patients early on, enabling timely intervention and improving prognosis.

During my PhD I have developed a keen interest in the neurobiology of psychosis and its relation to treatment response in first episode psychosis. Elucidating the underlying neurobiology of treatment resistance in psychosis could aid in better treatment selection and result in markers for earlier identification of these patients. The core focus of my PhD was the development and application of the novel neuromelanin-sensitive MRI (NM-MRI) technique as a potential clinical marker for treatment resistance. Additionally, I explored alternative markers, including plasma dopa decarboxylase activity as a blood marker and alterations in neurotransmitters, including glutamate and gamma-aminobutyric acid (GABA) levels. These markers hold significance for guiding treatment decisions, particularly in considering clozapine, the antipsychotic recognized for its superior effectiveness in treatment resistant schizophrenia.

At the SIRS 2022 conference, I had the honor to receive an early career award and to present the most notable finding from my PhD including a NM-MRI study in first episode psychosis patients. NM-MRI is a novel non-invasive MRI technique that indirectly measures dopamine functioning. In psychosis research, a common method for evaluating dopamine functioning is [18F]F-DOPA PET imaging, which has consistently shown increased activity in specific brain areas. Interestingly, treatment resistant patients do not show this increased dopamine functioning and show levels comparable to healthy individuals. Unfortunately, [18F]FDOPA PET imaging is expensive and relatively burdensome for patients, since it uses radioactivity and is administered intravenously, making it impractical for widespread use in screening for treatment resistance. NM-MRI as a proxy of dopamine functioning presents a promising alternative due to its non-invasive nature. NM-MRI shows increased signal in schizophrenia patients compared to healthy individuals, but had not yet been tested in treatment resistant schizophrenia. We aimed to determine whether treatment resistant patients show lower NM-MRI signal compared to patients who responded to antipsychotic medication. To accomplish this, we conducted a study in first episode psychosis patients, with a baseline and 6 month follow up measurement. In line with our hypothesis, treatment resistant patients showed significantly lower NM-MRI signal compared to responders, and similar NM-MRI signal compared to healthy individuals. Furthermore, NM-MRI appeared to be relatively robust as NM-MRI signal remained stable over six months follow-up and was not associated with illness duration, medication duration or dosage. These findings provide further evidence for dopaminergic differences between treatment resistant patients and responders, and support the potential of NM-MRI as a clinically applicable marker for treatment resistance in schizophrenia. This study has recently been published in the American Journal of Psychiatry and can be accessed online.

Following our findings that treatment resistant schizophrenia may be associated with a normal dopamine rather than an increased dopamine system, we redirected our attention to another neurotransmitter system: glutamate and GABA. These neurotransmitters are believed to play a role in treatment resistant schizophrenia. As a result, we aimed to further elucidate the roles of glutamate and GABA in the anterior cingulate cortex in first episode treatment resistant schizophrenia. I will present the results of this study as a poster at SIRS 2024 on Thursday.

Currently, I am a post-doctoral researcher at the Department of Psychiatry, Amsterdam UMC in the Netherlands. In this role I contribute to various projects, encompassing both neuroimaging and clinical studies in psychosis. Moving forward, I plan to expand my research endeavors while continuing to lend my expertise to other projects. Over the coming years, my goal is to deepen my understanding and experience in the field of psychosis. Eventually I want to use my accumulated expertise to pursue grants and establish my own research program dedicated to improving diagnostics and treatment for early psychosis.

My first contact with brain research was already in school in biology classes. The complex biology of the brain functioning was fascinating to me because of it’s many mysteries. When deciding what to study I always wanted to do research but also wanted to work on something that is directly related to people’s lives. The challenges in medicine seemed to fit these requirements. During my first internships I was intrigued by psychiatry and schizophrenia research. There were so many open questions and riddles to solve. So I started to do brain research at the Max-Planck Institute for Cognitive and Brain Sciences in Leipzig and then started my clinical career at Charité Berlin focusing on brain research in Schizophrenia. During my clinical routine I was fascinated by the extraordinary powers and abilities patients have. Although behavior sometimes is described as "non-functional" there is an enormous creativity and resilience in people with mental disorders. The multifactorial origins of those disorders have long puzzled researchers and clinicians alike. It’s multifaceted nature presents a significant challenge, but also an opportunity for innovation and discovery.

When I started my career, I embarked on a journey to unravel the intricacies of schizophrenia. I started with cutting-edge imaging technology and the goal for better understanding the human brain during crisis.  Neuroimaging techniques have revolutionized our ability to explore the complexities of the brain. Magnetic Resonance Imaging (MRI), Positron Emission Tomography (PET), and Functional MRI (fMRI) allow us to visualize the structure, function, and connectivity of neural circuits with unprecedented detail. These tools offer invaluable insights into the pathophysiology. I focused on alterations in glutamatergic and dopaminergic brain functioning, however, I was not completely satisfied and felt that despite decades of research, the underlying neurobiological mechanisms remain elusive, making diagnosis and treatment such a challenging task. I then delve more into the complex interaction of environmental factors and psychotic experiences. And landed in digital health to support patients in outpatient setting with innovative and effective tools. In addition to advancing our understanding of schizophrenia, technology has also revolutionized the way we support and empower patients. Digital tools and mobile applications have emerged as valuable adjuncts to traditional therapeutic approaches. These tools offer a wide range of functionalities, including symptom tracking, medication management, activation of resources and psychoeducation. One of the most significant advantages of digital tools is their ability to tailor interventions to the individual needs of patients. While the integration of digital tools into schizophrenia care holds immense promise, it is not without its challenges. Issues such as data privacy, accessibility, and the digital divide must be carefully addressed to ensure equitable access to these resources. Additionally, ongoing research is needed to validate the efficacy of these interventions and optimize their usability in clinical settings. In conclusion, the intersection of neuroimaging research and digital technology offers unprecedented opportunities to advance our understanding of schizophrenia and transform patient care. By embracing innovation and collaboration, we can navigate the challenges ahead and continue to support and empower patients during their recovery. While working in the field of schizophrenia research fostering interdisciplinary collaboration is what I enjoyed the most. 

I began studying genetics in my first year at Harvard, somewhat by accident. I had applied to be part of a seminar entitled “Chess and Mathematics,” but that course was filled, and I was bumped into “Darwin’s Finches”. I was disappointed, but not for long. I began to spend time in the archives of the Museum of Natural History, measuring the beaks of finches collected nearly 200 years ago, each with a tag tied to its leg with minute handwriting denoting the bird’s scientific name. Holding the birds that inspired the theory of evolution was the start of my fascination with genetics and classification. The next semester I moved to a synthetic biology wet lab, and after that to a drosophila lab at the Fred Hutchinson Cancer Research Center. At the same time, I was developing an interest in psychiatry and clinical psychology. My grandfather, who I idolized, was a psychiatrist. His son, who I never met, was diagnosed with schizophrenia. The family was unusually tight-knit, so my uncle’s absence was conspicuous, and highlighted how profoundly schizophrenia had impacted my father’s family of origin.  

I pursued a doctorate in clinical psychology at the University of Iowa because it presented the opportunity to pursue genomics research and clinical training in psychopathology. At both Iowa and the Minneapolis Veterans Affairs Medical Center, I was able to spend time with individuals who had experienced psychosis, working on inpatient, partial hospitalization, and outpatient treatment settings. When a postdoctoral opportunity arose on the Suffolk County Project, led by Drs. Roman Kotov and Evelyn Bromet and currently the longest-running study of first-admission psychosis in the world, I was thrilled to merge my research and clinical interests. My work with the project has focused on understanding how genetic risk factors manifest longitudinally over the 35 years the study has been running. We have shown that genetic risk can indicate who is more likely to experience a more severe course of negative symptoms. With the leaders of other first-episode studies, we are developing a consortium of longitudinal studies that can definitively evaluate how genetic risk impacts the course of symptoms, cognition, function, and response to treatment in psychotic disorders. 

In the past two years, I have developed an arm of research that aims to leverage what we know about the structure of psychosis to improve the power and precision of psychosis GWAS. Preliminary results from these analyses have confirmed the genetic structure of psychotic symptoms, mania, and depressive symptoms mirrors phenotypic structure, such that each genetic factor is relatively independent of the other. The support of the SIRS Early Career Award allowed me to present this work at the society’s 2022 meeting. A related line of research takes a broader approach, and tests whether transdiagnostic phenotypes of internalizing, externalizing, and psychosis, can identify more genetic risk factors than case-control GWAS. My hope is that this line of research will provide a clearer picture of psychotic disorders and the genetic risk factors associated with them, to facilitate the development of better diagnostic tools and treatments. 

My name is Théo KORCHIA, and I am a French psychiatrist, particularly involved in the treatment of early-onset schizophrenic disorders. 

First of all, I'd like to thank the Schizophrenia International Research Society for honouring me with this prestigious award, as well as the Faculty of Medical and Paramedical Sciences at Aix-Marseille University (France) and the Assistance Publique des Hôpitaux de Marseille (APHM), which supported me and enabled me to spend a year at McGill University in Montreal. 

Schizophrenia is a pathology often shrouded in mystery and prejudice, which profoundly affects the lives not only of those who suffer from it, but also those around them. 

Management of the first psychotic episodes determines the outcome and prognosis of patients, and it is therefore necessary to improve it. Generally speaking, my work highlights the value of pharmacogenetics, adapting and personalizing the antipsychotic treatment to different genetic profiles for greater efficacy. Consequently, various side-effects of antipsychotic therapy, notably sexual dysfunction which is very disabling and leads to discontinuation of treatment, are drastically reduced. Patient motivation must also be strengthened by including them in therapeutic decisions to improve overall quality of life. 

A particularly innovative aspect of my work concerns the impact of sexual dysfunction in patients suffering from schizophrenia. This issue, which has long remained on the fringes of psychiatric research, is crucial to patients' quality of life. Sexual dysfunction can be both a symptom of the illness and a side-effect of treatment, making it a dual challenge to overcome. 

My perseverance on this issue has led to the publication of a meta-analysis of over 21,000 patients worldwide, in the journal JAMA Psychiatry. 

Our study reveals with edifying clarity the high frequency of sexual dysfunction in individuals with schizophrenia spectrum disorders, showing an overall prevalence of 56.4%, with great variation in the types of dysfunction. This underlines the urgency of no longer neglecting adverse sexual effects in the treatment of schizophrenia. In the same way that weight gain or somnolence are side-effects commonly considered in the evaluation of antipsychotic treatments, it is crucial to include sexual dysfunction in our benefit-risk analysis. Recognizing and addressing these adverse effects goes beyond improving patients' quality of life; it represents a significant step forward in establishing a solid therapeutic alliance. Open communication about these issues, which are often stigmatized or played down, fosters a relationship of trust between doctor and patient, which is essential for effective management of schizophrenia. By taking these undesirable effects into account, we are improving not only adherence to treatment, but also the overall management of the patient, by recognising the importance of sexual health as a fundamental component of the patient's well-being. 

This study therefore represents a significant advance, opening-up new prospects for treatments that are more respectful and tailored to patients' needs. 

What drives my research is the conviction that innovation in psychiatry is not limited to the discovery of new drugs. It also lies in our ability to rethink the way we treat patients, by integrating dimensions of their experience that have been underestimated until now. The aim is twofold: to improve the quality of life of people suffering from schizophrenia and to reduce the obstacles to effective treatment, particularly those associated with the side effects of medication. 

The implications of the studies I lead aim to have a direct impact on clinical practice by providing healthcare professionals with the tools they need to build a solid therapeutic alliance, thereby encouraging adherence to treatment and improving clinical outcomes. Considering sexual dysfunction, and more broadly the side effects of antipsychotics, is a concrete example of this influence. 

My vision is of a dynamic psychiatry that is constantly evolving, where care is tailored to the uniqueness of each individual, and where each scientific advance lights the way towards better mental health. 

I am therefore grateful to be able to share with you not only my research objectives, but also my vision of a future in which the management of schizophrenia is more enlightened, more effective and, above all, more humane. The road is long, the challenges many, but the passion that drives my quest is unshakeable. With determination and perseverance, we can provide meaningful answers to those struggling with mental suffering, and open up new horizons for the psychiatry of tomorrow. 

Hyeon-Seung Lee

Individuals with depression often report their core belief of "I am worthless and unlovable." Individuals with anxiety disorders and OCD often report “what if” statement as a sign of excessive worry that leads to the thoughts of the worst-case scenario. Then, what would be a representative sign of schizophrenia? It is difficult to pick just one phenomenon given the multifaceted nature of the disorder, but I would pick "as if" statements related to the sense of self. Past research points out that self-disturbances are intertwined with the emergence of schizophrenia symptoms such as delusions and hallucinations. People at-risk often describe their experiences like this: “It feels 'as if' I am untuned to my body.” The anomalous feeling of altered self (agency, body ownership, self-boundary, and the experience of sensation, perception, and emotion) is a salient feature in the lives of those with schizophrenia. Bleuler’s original conceptualization of schizophrenia as that of the splitting of the mind and Kraepelin’s analogy of “an orchestra without a conductor” that indicates “a loss of inner unity”, both emphasize aberrations in the basic sense of self.  These self-disturbances have been shown to be important for predicting functional outcomes.  

Although the Research Domain Criteria (RDoC) of the National Institute of Mental Health (NIMH) and the International Classification of Diseases (ICD-11) include self-related features, self-disorder is not a prominent feature in either approach. Moreover, the sense of self has been ignored in the diagnosis, research, and treatment of schizophrenia due to lack of reliable and valid measures. With new methodological advances, it is now possible to empirically investigate the etiology and nature of self-disorders. As an early career researcher working with Dr. Sohee Park and multidisciplinary collaborators, I have developed and implemented novel experimental paradigms to elucidate and measure aspects of self-disturbances in schizophrenia. For instance, I have used virtual reality (VR) based measures to assess the neurocognitive representation of bodily space (i.e., peripersonal space) and how it is linked to schizophrenia symptoms. I also utilized VR-based social skills training to provide simulation and rehearsal of interpersonal interactions in realistic settings rather than explicitly teaching social cognitive skills to individuals with schizophrenia. In addition, I use computerized tools to visualize embodied emotions, manipulate cortical activities with brain stimulation, and assess the integrity of frontoparietal networks with neuroimaging to fully investigate the self-disturbances, symptoms, and social dysfunctions in schizophrenia. 

Specifically, my master’s thesis focused on the abnormal spatial self-consciousness in schizophrenia formed through multisensory processing. As objects or people approach one’s personal space, multisensory neurons in the frontoparietal brain facilitate appropriate reactions. I used VR-based multisensory integration tasks to identify the inflection point where multisensory reaction time is facilitated, which estimates the size and slope of personal space. I found that individuals with schizophrenia generate small but unclearly-defined personal space boundaries relative to controls in the social context. The size or shape of personal space was associated with the severity of negative symptoms and hallucinations. In an ongoing review study, I further demonstrated how personal space is altered in various mental disorders (e.g., anxiety, post-traumatic stress disorder, autism spectrum disorders, etc.). The personal space size is enlarged in various disorders; however, the self-space is more solidly formed in individuals with anxiety and autism spectrum disorders, while the boundary is unclearly generated in those with schizophrenia. My dissertation research further examines the altered representation of personal space, investigating the effect of threat, social distress, and socioemotional factors. 

Another line of research is investigating cross-cultural differences in the manifestation of psychosocial dysfunction. Previously, I examined the impact of the COVID-19 pandemic on the mental health of the general population from various cultures. Given the pandemic and social distancing were increasing feelings of social disconnection and loneliness, I expected that social disconnection and loneliness play a major role in poor physical and mental health. Delving into how cultural differences in public health strategies and compliance of the general population yield variances in reported stress, mood, anxiety, and psychotic experiences provided me with either a microscopic or a macroscopic view of psychosocial dysfunction. Moreover, I investigated culture-general and specific aspects of mental health symptoms and abnormal self-related experiences in schizophrenia. Previous cross-cultural works highlighted that though symptoms and self-disturbances are salient and prevalent in both Western and non-western cultures, there were culture-specific aspects such as relatively high tolerance for anomalous self-experiences and less attenuated embodied emotion in Koreans. I would like to continue to investigate cultural effects on psychosocial functions. 

Psychiatric research is still mostly driven by researchers from Europe and North America. As a Korean scientist, I believe we have valuable contributions to make to this field and I hope to increase the representation of Korean and other Asian scientists in the field of schizophrenia research. Increased diversity of ideas and approaches will surely positively impact the future of the Schizophrenia International Research Society (SIRS).