Tuesday, June 24: 17:30 - 19:30
BCEC
Room: Great Hall
Since 2009, the ENIGMA Consortium has brought together over 2,000 brain researchers from 47 countries to coordinate the largest neuroimaging studies of over 30 brain diseases – a global effort driven by the expertise and vision of many in this very audience. This global alliance reflects the shared vision, mutual support, and collective power of the neuroimaging community, to tackle questions that no single lab can address on its own. ENIGMA began by tackling the replication crisis in brain imaging genetics, uncovering over 500 common and rare genetic and epigenetic variants that influence brain structure, function, and the speed of brain aging (Grasby et al., Science, 2020; Brouwer et al., Nature Neuroscience, 2022). These findings laid the groundwork for broader studies: today, ENIGMA’s 30 disease-focused working groups coordinate the largest MRI, DTI, and fMRI studies in psychiatry (e.g., schizophrenia, bipolar disorder, major depression, PTSD, addiction, OCD), neurology (e.g., epilepsy, Parkinson’s, ataxia, neuro-HIV, TBI, chronic pain), and several neurodevelopmental brain disorders (anorexia, conduct disorder, Tourette syndrome, neurogenetic syndromes). By applying rigorous, consensus-driven workflows to vast global datasets, ENIGMA is revealing unexpected disease subtypes, risk factors, and treatment effects, identifying emerging principles that connect and distinguish multiple brain disorders, linking to neuroscientific findings at cellular and molecular scales (Larivière et al., ENIGMA Toolbox, Nature Methods, 2021).
ENIGMA’s impact extends globally through initiatives such as ENIGMA India, Pakistan, and the ENIGMA-U education program, fostering open collaboration, training, and opportunities for all. In this talk, we will outline major findings to date and examine how AI-driven methods may reshape the landscape of brain research. With generative AI, vision-language models, and multimodal brain decoding, we are on the cusp of new possibilities – from decoding disease mechanisms to designing targeted treatments. The global quest to alleviate brain diseases is within our reach – a collective endeavour that is greatly empowered by the OHBM community, supporting us all in our shared mission to bring life-changing discoveries to all corners of the globe.
Keynote Speakers

Professor
School of Psychological Sciences, Monash University Australia
Wednesday, June 25: 10:30 - 11:15
BCEC
Room: Great Hall
Understanding how the brain flexibly reconfigures its connectivity across time, space, and context is a major goal in systems neuroscience. In this talk, I will present recent advances in generative modelling of brain connectivity developed to address this challenge using multimodal neuroimaging data. Building on the framework of Dynamic Causal Modelling, I will introduce novel approaches that integrate functional MRI, diffusion imaging, and electrophysiological recordings to infer hidden neuronal states and directed interactions across brain regions. These methods offer a principled way to combine anatomical constraints with dynamic functional measurements, enabling more accurate and mechanistically interpretable models of brain function. I will also briefly describe a complementary foundation model that learns robust, interpretable brain representations by fusing time series, structural, and effective connectivity data using transformer-based architectures.
In the second part of the talk, I will demonstrate the application of these tools to altered states of consciousness, focusing on new findings from PsiConnect, the largest multimodal imaging study to date of the acute psychedelic state. Combining multi-echo fMRI and 64-channel EEG across systematically varied sensory and psychological contexts, we identify a structured shift from sensory-driven to associative cortical processing under psilocybin. Using advanced connectivity analyses and machine learning, we uncover a reproducible neural signature of the psychedelic state that tracks with subjective experience and predicts therapeutically relevant outcomes at the individual level. Contrary to the view of psychedelics as inducing disordered brain activity, our findings reveal a coherent, context-sensitive reorganisation of cortical dynamics. We introduce embeddedness as a mechanistic framework for integrating internal and external perception, offering a novel perspective on how transient altered states can lead to sustained psychological change. Together, this work bridges advances in generative modelling, neuroimaging, and psychedelic science to inform both theories of brain function and the future of personalised mental health interventions.

Assistant Professor
University of Wisconsin-Madison
Wednesday, June 25: 16:45 - 17:30
BCEC
Room: Great Hall
What is consciousness, and what is its neural substrate in the brain? Why are certain parts of the brain important for consciousness, but not others that have even more brain cells and are just as complicated? Why does consciousness fade with dreamless sleep even though the brain remains active? Does consciousness always fade when patients become unresponsive after brain damage, during generalized seizures, during general anesthesia, or even in deep sleep? And are newborns, animals, and intelligent computers conscious? Integrated information theory (IIT) is an attempt to answer these and other questions in a principled manner. IIT starts not from the brain, but from consciousness itself – by identifying phenomenological properties that are true of every conceivable experience. It then uses a causal mathematical framework to translate these phenomenological properties into predictions about physical properties that a system should have to be conscious. As a next step, IIT uses the same consciousness-first, causal approach to also generate predictions about neural substrates that can support specific experiences such as spatial extendedness, temporal flow, hierarchical/categorical contents, and modality-specific qualities such as colors and sounds. The results of this exploration can account for many empirical findings, lead to counterintuitive predictions that can be challenged by neuroscientific experiments, and has motivated the development of promising new tests for the practical assessment of consciousness in non-communicative patients.
Postdoctoral Research Scientist
Universidade do Minho
Thursday, June 26: 10:30 - 11:15
BCEC
Room: Great Hall
This keynote examines our tendency to interpret correlated brain activity as evidence of neuronal interactions. While functional networks have become a cornerstone of modern neuroscience, this talk explores whether long-range correlations in brain activity necessarily reflect the propagation of information through axonal connections. I will discuss alternative explanations for these correlated patterns, including principles from wave physics, biomechanics, and fluid dynamics, which may drive similar macroscale dynamics yet not relying on axonal pathways. By reconsidering the nature of functional networks, we can develop models that better explain how these activity patterns support healthy cognition and how their disruption may lead to cognitive impairments and psychiatric symptoms. This perspective doesn't invalidate the wealth of functional connectivity research, but rather enhances our interpretive framework and opens new avenues for advancing our understanding of brain activity at the scales captured with fMRI and its role in mental health.

Senior Scientist & Director
Italian Institute of Technology
Thursday, June 26: 17:15 - 18:00
BCEC
Room: Great Hall
Human brain disorders are characterized by dysfunctional communication among brain regions. Yet, the biological mechanisms underlying this “functional dysconnectivity” remain unclear. In my talk, I will highlight recent cross-species research aimed at decoding patterns of brain dysconnectivity into their molecular and neurophysiological underpinnings. In particular, I will illustrate how targeted perturbational approaches can reveal fundamental physiological principles underlying the organization of large-scale functional connectivity, and its disruption in brain disorders. By bridging findings across species and investigational scales, this emerging approach opens new avenues for modelling and interpreting functional connectivity in both healthy and in neuropathological states.
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Professor
Hong Kong Polytechnic University
Friday, June 27: 10:30 - 11:15
BCEC
Room: Great Hall
This talk explores the profound influence of fetal programming, where in-utero experiences shape long-term neurodevelopmental and mental health outcomes. We will examine how maternal psychological stress during pregnancy alters fetal brain development, increasing susceptibility to psychopathology across the lifespan. Drawing from our comprehensive longitudinal cohort study, we will highlight the intricate relationship between maternal mental health and child brain development, emphasizing the role of early-life environmental exposures. Additionally, we will discuss how genetic factors interact with prenatal and postnatal environments to modulate neurodevelopmental trajectories. Finally, we will introduce advances in AI-driven predictive models for early identification of mental health risks and explore potential intervention strategies aimed at fostering resilience and improving child mental health outcomes.

Professor
Semel Institute for Neuroscience and Human Behavior
Friday, June 27: 17:15 - 18:00
BCEC
Room: Great Hall
While the idea that the human brain is composed of multiple large functional networks has been gaining traction in cognitive and network neuroscience, the field has yet to reach consensus on
several key issues regarding terminology. What constitutes a functional brain network? Are there “core” functional networks, and if so, what are their spatial topographies? What naming conventions, if universally adopted, will provide the most utility and facilitate communication amongst researchers? Can a taxonomy of functional brain networks be delineated? The Workgroup for HArmonized Taxonomy of NETworks (WHATNET) was formed in 2020 as an OHBM–endorsed best practices committee to provide recommendations on points of consensus, identify open questions, and highlight areas of ongoing debate in the service of moving the field toward standardized reporting of network neuroscience results. The group has developed a Network Correspondence Toolbox (NCT) to permit researchers to examine and report spatial correspondence between their novel neuroimaging results and multiple widely used functional brain atlases. The adoption of the NCT will make it easier for researchers to report their findings in a standardized manner, thus aiding reproducibility and facilitating comparisons between studies to produce interdisciplinary insights.

Associate Professor
School of Psychological Sciences, Monash University Australia
Saturday, June 28: 10:30 - 11:15
BCEC
Room: Great Hall
Relative to other organs in the human body, the brain relies upon a large energy budget, which is primarily met through the metabolism of glucose. This reliance on glucose shapes both the anatomical organisation of the brain network as well as its functional efficiency. A reliable and scalable (i.e., able to be up- and down-regulated on demand) supply of glucose is necessary for brain health, and changes in cerebral glucodynamics results in cognitive dysfunction, psychiatric illness and neurodegenerative disease. Coherent glucodynamic signals across the brain form a functional metabolic network that primarily reflects postsynaptic signals of information transfer in the brain.
In this presentation, I will discuss recent advances in understanding the dynamic nature of cerebral glucose metabolism and the metabolic network of the brain. By drawing upon simultaneous PET/MR data, I will demonstrate that the metabolic network of the brain provides unique and complementary insight into the functional organisation of the brain compared to the fMRI-derived functional network. Finally, I will discuss how glucodynamics and the metabolic network of the brain matures across the healthy adult lifespan.