Dr. Mateus Vidigal de Castro is a postdoctoral researcher at the University of São Paulo, Brazil. His research focuses on the cellular and molecular mechanisms underlying healthy aging, disease resilience, and extreme longevity. He leads studies involving induced pluripotent stem cells (iPSCs) derived from centenarians, aiming to better understand the biology of aging and its intersection with infectious diseases such as COVID-19. Dr. de Castro is also a member of Sigma Xi, the Scientific Research Honor Society. He is particularly passionate about exploring how genetic diversity in underrepresented populations can reveal novel insights into longevity and human health. In this Genomic Press Interview, Dr. de Castro shares with our readers his reflections on his life, career, and the scientific journey that continues to inspire him.
Dr. Mirko Manchia is an Associate Professor of Psychiatry at the Department of Medical Sciences and Public Health of the University of Cagliari, Cagliari, Italy, and holds an adjunct appointment in Pharmacology at Dalhousie University, Halifax, Nova Scotia, Canada. Dr. Manchia's research examines the genetic basis of bipolar disorder and other related complex traits such as response to long-term treatment with lithium and suicidal behavior. His work is not only of theoretical interest but also clinically relevant. One such example was the publication in the Lancet of genome-wide significant association signals for lithium response in a large cohort of bipolar patients (Hou et al. 2016) performed in the context of the international consortium on pharmacogenetics of lithium response (ConLiGen) of which Dr. Manchia is a co-investigator and founding member. In addition, he was responsible for the phenotypic analysis of the sample (Manchia et al., 2013). During his career, Dr. Manchia has established an excellent track record, having published 230 papers to date in international peer-reviewed journals on molecular genetics and the clinical aspects of bipolar disorder. He is an active Principal Investigator (PI) of research projects funded by EU and national agencies, and he is also involved in several other international consortia, including PGC-BD. He is the chair of the European College of Neuropsychopharmacology (ECNP) Bipolar Disorders Network. Furthermore, he serves as the Senior Editor for Neuroscience Letters and is an associate editor for several international Journals. Dr. Manchia has successfully combined molecular-genetic and statistical methods with a clinical understanding of research problems in psychopharmacology and pharmacogenomics. In this Genomic Press Interview, Dr. Manchia is delighted to provide our readers with reflections on his life and career.
In this illuminating Genomic Press Interview, Dr. Xuyu Qian, a visionary neuroscientist whose groundbreaking spatial transcriptomics research promises to revolutionize our understanding of human brain development at unprecedented single-cell resolution, shares his remarkable path from an art-infused childhood in Nanjing to becoming a Forbes 30 Under 30 laureate and pioneering force in brain organoid technology. As the newly minted Assistant Professor at the University of Pennsylvania and Children's Hospital of Philadelphia, Dr. Qian has transformed our understanding of human cerebral cortex formation through his innovative fusion of spatial transcriptomics and organoid models. His landmark work, recently published in Nature (2025), leveraged state-of-the-art MERFISH technology to analyze over 18 million single cells, thereby redefining our understanding of the emergence of cortical layers and specialized brain regions during fetal development. This breakthrough builds upon his earlier revolutionary development of brain organoid protocols, now cited over 2,000 times and instrumental in shaping CDC guidelines for the prevention of Zika virus. Throughout this candid conversation, Dr. Qian reveals how the anime series Evangelion sparked his passion for biotechnology, explores his generous collaborative philosophy that has led to numerous discoveries, and articulates his commitment to human-centric approaches for decoding neurodevelopmental disorders. His distinctive combination of scientific excellence, creative vision, and infectious enthusiasm establishes him as one of neuroscience's most promising emerging leaders, destined to unravel the fundamental mysteries of human brain development and disease.
Eric D. Sun illuminates the revolutionary intersection of machine learning and aging biology, which promises to transform our understanding of brain aging at an unprecedented single-cell resolution. Emerging from Stanford University's Biomedical Data Science program, Eric Sun is set to establish his independent laboratory at MIT's Department of Biological Engineering and the Ragon Institute in 2026. He represents the vanguard of computational scientists redefining aging research through innovative artificial intelligence approaches. His groundbreaking development of spatial aging clocks, sophisticated machine learning models capable of measuring biological age at the cellular level, has unveiled previously hidden mechanisms of brain aging, including the remarkable discovery of cell types that can dramatically influence the aging trajectory of neighboring cells in both pro-aging and pro-rejuvenating directions. This pioneering work, recently published in Nature (2025), bridges the gap between computational innovation and biological discovery, positioning Eric Sun at the forefront of a new era in aging research where machine learning not only decodes the complex biology of aging but also accelerates the discovery of targeted interventions against age-related diseases, including dementia. Through this compelling Genomic Press Interview, readers gain intimate insights into the scientific journey, philosophical perspectives, and ambitious vision of a rising star whose multidisciplinary approach promises to unlock the secrets of healthy brain aging and translate these discoveries into transformative therapeutics for humanity's most pressing age-related challenges.
Polygenic scores (PGS), summarizing the cumulative contribution of common genetic variants to psychiatric phenotypes, are increasingly investigated as putative predictors of treatment response and illness course. In major depressive disorder (MDD), several studies have associated higher MDD PGS with a modestly increased risk of nonresponse, lower remission rates, and treatment resistance. Conversely, bipolar disorder (BD) PGS have yielded more heterogeneous findings, with largely null or weak associations in unipolar depression but a possible on lithium response in BD cohorts, while lower MDD PGS showed a more consistent beneficial effect on lithium response in BD. MDD PGS may also have a modulating effect on clinical features of schizophrenia and a range of other psychiatric disorders. Nonetheless, the variance explained remains limited and predictive power improves only marginally when PGS are used in isolation. Integrative approaches that combine clinical predictors, environmental measures, and biomarker data appear to enhance prediction over genetics alone, which is increasing due to the most recent large genomewide studies. However, ancestral diversity remains limited, with most research conducted in Caucasian samples. Taken together, current evidence supports the incremental value of MDD and BD PGS in informing prognosis and treatment response, though clinical implementation remains premature. Replication in ancestrally diverse samples, integration with dimensional phenotypes, and improved modeling strategies will be essential to translate genetic liability into clinically actionable insights in precision psychiatry.
The relationship between leptin and interleukin 1 receptor antagonist (IL1RA) is critical to the understanding of obesity's low-grade chronic inflammatory state. IL1RA antagonizes the proinflammatory effects of IL1, dampens systemic inflammation markers, and in clinical trials improved glycemic control in type 2 diabetes. We show that leptin levels decreased relative to the number of Il1rn copies in mice overexpressing IL1RA; these mice have altered white fat distribution with decreased epididymal and retroperitoneal fat tissue masses. They also have increased IL1RA plasma levels and insulin sensitivity. Recombinant IL1RA may be a novel treatment strategy for metabolic syndrome by improving resistance to leptin and insulin.
In this Genomic Press Interview, Professor Barbara Franke, a trailblazing molecular psychiatrist at Radboud University in Nijmegen, shares her extraordinary scientific journey from an inquisitive child fascinated by nature to becoming one of the world's most influential researchers in biological psychiatry. With over 500 peer-reviewed publications and recognition among the top 1% most cited scientists globally, Franke has helped to revolutionize our understanding of the genetic foundations of neurodevelopmental disorders, particularly ADHD. Bringing together international experts for interdisciplinary research, she founded and leads multiple international research consortia, including the International Multicentre persistent ADHD Collaboration (IMpACT) and the ECNP Network ADHD across the lifespan. Her pioneering work extends beyond gene identification to illuminating the biological pathways from genetic variations to altered behaviour, employing innovative complementary approaches including bioinformatics, brain imaging genetics, and experimental models using fruit flies and human induced pluripotent stem cells. An elected member of the Royal Netherlands Academy of Arts and Sciences, decorated Knight in the Order of the Netherlands Lion, and recipient of numerous prestigious awards, Franke's scientific contributions are matched by her passionate commitment to international collaboration and mentorship of the next generation of researchers. Her recent move into epigenetics research, investigating the interplay between heritable and environmental influences on psychiatric conditions, illustrates her unwavering determination to contribute to a new nosology in psychiatry that will ultimately improve diagnosis, treatment, and management for millions worldwide. Guided by the German proverb “Die Suppe wird nicht so heiß gegessen, wie sie gekocht wird” (“The soup is not eaten as hot as it is cooked”), Franke's balanced approach to life and science continues to inspire groundbreaking advances at the intersection of genetics, neuroscience, and psychiatry.
Botulinum neurotoxins (BoNTs) block cholinergic signaling at neuromuscular junctions, inducing transient muscle paralysis while avoiding neuronal death. However, the mechanism(s) underlying these dual features are yet unknown. Here, we report accumulation of 5'Lys transfer RNA fragments (tRFs) in both BoNT/A-intoxicated cultured human neuroblastoma cells and submandibular glands from BoNT/A-intoxicated rodents. Importantly, we show that 5′LysTTT tRFs balance ferroptosis by cointeracting with the RNA-binding ferroptosis-inducing protein HNRNPM and the 3' untranslated region of the ferroptosis-inhibiting CHAC1 mRNA. Moreover, approximately 20% of the BoNT/A-induced tRFs shared an 11-nucleotide-long LysTTT and LysCTT tRFs-included motif, CCGGATAGCTC, which may target transcripts containing complementary sequences, including the UNC5B transcript that can regulate cell survival. Collectively, the multiple regulatory roles of tRF-5′LysTTT and the shared repetitive motif reveal mechanism(s) supporting the survival of cholinergic neurons under BoNT/A exposure. This understanding may predict the development of novel BoNT/A therapeutic avenues for treating diverse neuromuscular disorders and BoNT/A cosmetic procedures.
Prader-Willi syndrome (PWS) is a complex neurodevelopmental genetic disorder caused by the absence of paternal gene expression within the PWS critical region (15q11-q13) on chromosome 15. The loss of gene function can result from deletion, maternal uniparental disomy, or imprinting center defects. Occurring equally in both sexes, PWS is characterized by a spectrum of physical, behavioral, and cognitive symptoms, including hyperphagia and obesity, and presents with various co-occurring psychiatric conditions such as autism spectrum disorder (ASD) and psychotic spectrum disorders (PSD). Approximately 12%–40% of individuals with PWS meet the criteria for ASD, while a smaller subset, around 10%–30%, may develop PSD in late adolescence or adulthood. The treatment of PWS typically involves a multidisciplinary approach, including behavioral interventions to manage hyperphagia, growth hormone therapy to address its deficiency, and pharmacological treatments for psychiatric symptoms. Additionally, there is growing interest in genetic and molecular therapies as potential future interventions. By integrating clinical, neurobiological, and genetic findings, this review highlights the implications of PWS for understanding co-occurring development, psychiatric disorders, and therapeutic potential through new intervention models.
This commentary examines recent findings demonstrating that individuals with depression exhibit a functionally expanded salience network compared to non-depressed controls. Neuroimaging data reveals this network expansion predates symptom onset and remains stable regardless of symptom severity or treatment interventions. The authors propose this distinctive neural signature as a potential biomarker for depression risk, enabling earlier identification and intervention. They discuss three potential mechanisms underlying this expansion: compensatory network changes, genetic predisposition, and relative expansion secondary to atrophy in other brain regions. The commentary emphasizes the need to conceptualize depression as a disorder of neural connectivity rather than isolated neurotransmitter imbalances, with implications for developing targeted therapeutic approaches.
Spanning over four decades at France's premier research institutions (CNRS and INSERM), Dr. Yehezkel Ben-Ari's groundbreaking neuroscience research has fundamentally transformed our understanding of brain development through his seminal discovery of the GABA excitatory-to-inhibitory developmental shift, an evolutionary conserved principle later validated across all species from worms to humans. After directing the INSERM unit at Port-Royal Maternity and founding the Mediterranean Institute of Neurobiology (INMED), Ben-Ari's unexpected observation of GABA's paradoxical excitatory role in immature neurons, which he initially set aside for over a year before recognizing its significance earned him prestigious recognitions including the Grand Prix INSERM, the Milken award of the Epilepsy Foundation of America (EFA) and an award from the European Society of Epilepsy. In this Genomic Press Interview, Ben-Ari reflects on his scientific journey, including his transition after French mandatory retirement to founding innovative therapeutic ventures targeting autism spectrum disorders, epilepsy, and brain tumors based on his unifying “Neuroarcheology” concept, proposing that many neurological disorders stem from developmental mechanisms that can be targeted with specific medications like bumetanide, which has shown promising results in clinical trials by modulating chloride transporters. While continuing to teach at the Pasteur Institute's brain development doctoral program, Ben-Ari's career exemplifies how persistence in investigating unexpected observations can lead to transformative discoveries with profound clinical implications, bridging the gap between fundamental neuroscience research and innovative therapeutic applications for previously untreatable neurological conditions.
Abnormal α-synuclein aggregation is a pathological hallmark of Parkinson's disease, multiple system atrophy, and dementia with Lewy bodies. A suitable radiotracer that can noninvasively map synucleinopathies through positron emission tomography (PET) will lead to breakthroughs in early diagnosis, monitoring disease progression, and evaluating treatment responses. However, the development of PET tracers for α-synuclein is lagging due to several challenges. In this perspective, we provide a brief review of the advancements in PET tracers targeting α-synuclein and summarize recent clinical studies aimed at mapping synucleinopathies in neurodegenerative patients using these PET tracers.
Dr. Carrie E. Bearden is a Professor of Psychiatry and Biobehavioral Sciences and Psychology at the University of California, Los Angeles (UCLA). Dr. Bearden received her Ph.D. in Clinical Psychology from the University of Pennsylvania and completed her clinical training at UC San Diego. She joined the UCLA faculty in 2003. Her work aims to understand neurobiological risk factors for the development of severe mental illness in youth, both in clinically defined high-risk cohorts and in highly penetrant genetic conditions. She is particularly known for her research taking a 'genetics first' approach to studying brain mechanisms underlying the development of severe mental illness. Dr. Bearden is the Director of the UCLA Center for Assessment and Prevention of Prodromal States (CAPPS), a clinical research program for youth at high risk for psychosis and Co-director of UCLA's Neurogenetics Training Program. She has over 350 peer-reviewed publications and is among the world's most highly cited scientists, according to Clarivate, Web of Science. Currently, she serves as Deputy (Reviews) Editor for the journal Biological Psychiatry, as Chair of the DSM-V Serious Mental Disorders Committee and is President-Elect of the Society of Biological Psychiatry. She has received numerous awards and honors, both for her research achievements and for teaching and mentorship, including the Joel Elkes Research Award (ACNP), the A.E. Bennett Neuropsychiatric Research Award (Society of Biological Psychiatry), and an NIH Method to Extend Research in Time (MERIT) award. Professor Bearden is delighted to engage in the Genomic Press Interview, sharing insights about her personal and professional journey with our readers.
As a distinguished James McGill Professor and now Professor Emeritus at McGill University, Michael Meaney's scientific journey is a testament to the power of curiosity in science. His fascination with how our environment shapes our genes, brain function, and mental health has led to discoveries that have changed how we think about human development. After leading groundbreaking research at McGill, he took his expertise to Singapore, where, as Director of the Translational Neuroscience program at ASTAR, he helped shape the innovative GUSTO birth cohort study. His profound impact on neuroscience is reflected not just in his impressive collection of honors – from the Order of Canada to his recent election to the American Academy of Arts and Sciences – but in how his work has touched lives. With over 650 publications to his name, Meaney has helped bridge the gap between molecular biology and public health. We are fortunate to have him share his insights with our readers in this Genomic Press Interview.
When Genomic Press started, I never imagined our defining moment would come from a children's book. Yet here we are, finding our soul in the story of a lonely color that could not fit in. I remember the first time I encountered Flicts. I was an adult and a good friend gave me the book with a knowing smile. “Trust me,” she said, “this will make sense.” She was right, though not in any way I could have anticipated.Finding Our Place: The Flicts Story and the Heart of Genomic Press
Ziraldo: The Godfather of
Peter Falkai stands as one of the world's leading authorities in psychiatric research, particularly in understanding the neurobiology of schizophrenia. As a Scientific Member of the Max Planck Society and Director and Head of the Hospital at the Max Planck Institute of Psychiatry since October 2024, he continues to advance our understanding of mental health disorders. His distinguished career spans over three decades, during which he has held multiple prestigious leadership positions, including President of the European Psychiatric Association (2021–2023) and current President of the World Federation of Societies of Biological Psychiatry. A member of the German Academy of Sciences Leopoldina, where he served as Senator of the Neurosciences Section, Prof. Falkai has been instrumental in shaping modern psychiatric research and treatment approaches. His groundbreaking work on brain plasticity and innovative treatment combinations has opened new pathways for understanding and treating psychotic disorders. As site spokesperson for the German Centre for Mental Health and former President of the German Society for Psychiatry and Psychotherapy, Psychosomatics and Neurology, he continues to bridge the gap between basic research and clinical application. In this Genomic Press Interview, Prof. Falkai graciously shares insights into his remarkable professional journey and personal life, offering readers a glimpse into the mind of one of psychiatry's most influential figures.
Our modern syndrome of major depression developed over the 19th century and assumed its largely current form in Europe during the last decades of that century. A defining monograph in that historical development in German-speaking Europe was published by Krafft-Ebing in 1874. In this article, we provide a detailed commentary (and an English translation) of key sections of a monograph—“La Mélancolie” (The Melancholy) published by Roubinovitch and Toulouse in 1897—that plays a parallel role in the Francophone world. We emphasize six features of this important document. First, is it thoroughness, covering, with often vivid descriptions, the symptoms, signs, subtypes, course of illness, and outcome of melancholia. Second, this work describes the key features of the evolution of the concept of melancholia over the prior century. Third, we also see in this monograph important references to the leading explanatory psychophysiological model for melancholia developed in the middle third of the 19th century—melancholia as psychalgia or “mental pain.” Fourth, the authors are committed to attempting to understand, in psychological terms, key features of the melancholic syndrome and in particular the development of delusions. Fifth, they give great emphasis to a symptom/sign pair in their diagnosis and description of melancholia: psychological suffering accompanied with resignation and “psychophysical decrease.” Sixth, these authors attend to the lived experienced of their melancholic patients, considering some key themes, such as derealization, now emphasized in phenomenological studies of depression. Seventh, they have an insightful view of the evolution of psychiatric diagnoses that applies to the modern day—that disease identification in psychiatry lags behind that most parts of medicine as our diagnostic categories are still “only provisional symptomatic groupings which will one day be replaced by more exact conceptions of the nature of the relationships which unite the facts.”
Philippe Courtet is a distinguished figure in psychiatry and suicidology who has significantly contributed to the field. As an influential PU-PH (Professeur des Universités-Praticien Hospitalier), he is a Professor of Psychiatry at the University of Montpellier, France, and head of Emergency Psychiatry at the University Hospital of Montpellier. Leading the Chair of Excellence in suicide prevention at the Fundamental Foundation and the ‘biomarkers, environment and neuropsychiatry’ research group at the National Institute of Health and Medical Research (Institut National de la Santé et de la Recherche Médicale, INSERM), Professor Courtet has focused on understanding the vulnerability to suicidal behaviour in mood disorders. His innovative work combines genomics, brain imaging, and social research. With over 500 peer-reviewed articles, an H-index of 82, and 27,000 citations, he stands as one of France's most productive psychiatrists and an international leader in suicidology. His role as Chair of the Suicidology and Suicide Prevention Section of the European Psychiatric Association further cements his influence in the field. Professor Courtet's groundbreaking research and dedication to improving care through the development of connected health tools for suicide risk assessment underscore his commitment to advancing treatment. We are pleased that Professor Courtet has participated in an exclusive Genomic Press Interview, which he entitled “Hell is other people.1” How social pressure shapes suicidal thoughts, offering our readers unique insights into his life and vision for the future of psychiatry and suicide prevention.
Robin Dunbar is an eminent evolutionary psychologist and anthropologist whose pioneering work has permanently redefined how we think about human social relationships. Dunbar, who is an emeritus Professor of Evolutionary Psychology at the University of Oxford, became world-renowned for, among other contributions, his formulation of “Dunbar's number,” a theoretical limit to the number of stable social relationships an individual can maintain, typically cited as about 150. That idea, which he developed as he studied the relationship between brain size and social group size in various primate species, has since had broad influences across areas from social media design to organizational management. Over time, Dunbar's number has become more widely known and discussed, particularly with the advent of social media and online social networks. This has led to renewed interest in its implications for digital social interactions. Dunbar's illustrious career spans multiple prestigious institutions, including, prior to joining Oxford in 2007, the University of Cambridge, the University of Stockholm (Sweden), University College London and the University of Liverpool. He is a fellow of the British Academy and the Royal Anthropological Institute, a Foreign Member of the Finnish Academy of Science and Letters, and an elected Honorary Member of the Hungarian Academy of Sciences. His interdisciplinary expertise is reflected in his professorships in psychology, evolutionary biology, and anthropology at institutions such as Liverpool and Oxford Universities. He has held a visiting chair in statistical physics and computer science at Aalto University, Finland, which has also awarded him an honorary doctorate. Dunbar studies the evolution of social processes in primates and humans, with work that blends neurobiology, cognitive science, and the social dynamics of how we communicate via friendship networks. His insights into friendships and community cohesion continue to shape our understanding of human social behaviour in the digital age. It is an absolute pleasure that Professor Dunbar answered the Genomic Press Interview as we celebrate the extraordinary story of his scientific odyssey with our readers.
Dr. C. Robert Cloninger's contributions have been foundational in understanding temperament, personality, and their biological and genetic underpinnings. Cloninger explored how temperament, character, and personality traits are influenced by genetic factors and how they predict various psychological disorders, such as alcoholism and personality disorders. His prospective studies involving adoptees reared apart from their biological parents provided crucial insights into the heritability and development of personality traits independent of environmental influences. Moreover, Cloninger's pioneering work in conducting the first genome-wide association and linkage studies of normal personality traits laid the groundwork for subsequent research in psychiatry and behavioral genetics, linking specific genetic profiles to patterns of temperament and personality. He is also the creator of two extensively employed personality assessment instruments: the Tridimensional Personality Questionnaire (TPQ) and the Temperament and Character Inventory (TCI). Dr. Cloninger serves as Director of the Anthropedia Institute and Professor Emeritus at Washington University in St. Louis, where he studies the biopsychosocial foundations of personality that influence health and illness. The Anthropedia Institute is the research branch of the Anthropedia Foundation, a non-profit organization dedicated to the promotion of human well-being through initiatives in health care and education. He served as Wallace Renard Professor of Psychiatry & Genetics, Professor of Psychological and Brain Sciences, and founding Director of the Sansone Center for Well-being at Washington University until July 2019. Dr. Cloninger is a member of the National Academy of Medicine USA, Fellow of the American Academy for Advancement of Science, and an editor of various journals in psychiatry, psychology, and genetics. We are pleased to share Dr. Cloninger's answers to the Genomic Press Interview.
Dr. Yoshikawa currently serves as the Administrative Director of the RIKEN Center for Brain Science in Japan. His journey with the institution began in 1999 when he assumed the Principal Investigator (Team Leader) role and established the Laboratory of Molecular Psychiatry. Before this, he gained experience at various esteemed institutes, including the Department of Psychiatry at Tokyo Medical and Dental University, the National Institute of Physiology in Japan, and the National Institute of Mental Health (NIMH) in the USA. For 22 years, Dr Yoshikawa dedicated himself to unraveling the molecular intricacies of psychiatric diseases within his laboratory. Transitioning to his current position, he now lends his expertise to the operational endeavors of the Center. Beyond his administrative responsibilities, Dr. Yoshikawa actively engages with the academic communities, serving as a grant reviewer, scientific advisor, and editorial board member for scientific journals. Remarkably, he maintains his clinical practice, caring for patients as a psychiatrist. Dr Yoshikawa graciously participated in the Genomic Press interview, sharing insights into his life and career and providing valuable reflections for our readers.
