26.04.2026, Sunday, 12:30-14:00
General focus of the symposium:
This symposium will focus on emerging concepts and methodologies that frame inflammation as a dynamic and spatially organized process in the injured and diseased brain. By bringing together expertise in microglial biology, peripheral immune mechanisms, and advanced spatial profiling technologies, the session aims to explore how resident and infiltrating immune cells interact to shape local and peripheral inflammatory responses. Emphasis will be placed on ischemic stroke as a model of acute brain injury, with broader relevance to other neurological and neurodegenerative disorders. Neuroinflammation plays a fundamental role in brain injury and disease, influencing tissue damage, repair processes, and long-term neurological outcomes. Rather than representing a uniform immune response, neuroinflammation emerges from highly dynamic and spatially structured interactions between resident microglia and infiltrating peripheral immune populations. Understanding how these immune networks are initiated, regulated, and maintained within the brain and beyond is critical for identifying mechanisms that promote either recovery or disease progression, as well as to minimize secondary complications.
A central theme of the symposium will be microglial heterogeneity and immune cell communication within and beyond the central nervous system. Speakers will discuss microglial response after brain injury, their crosstalk with peripheral innate immune cells, and the systemic immune consequences of stroke. The session will highlight how these interactions regulate neuroinflammatory responses and influence tissue remodeling, functional recovery, and even secondary immunological complications beyond the neurological consequences.
In parallel, the symposium will emphasize methodological advances that are transforming the field of neuroimmunology. Speakers will highlight techniques such as single-cell transcriptomics, single-cell epigenomics, and high-dimensional spatial profiling approaches, including imaging mass cytometry and related spatial proteomic technologies, which enable immune responses to be analyzed in depth directly, and even within intact tissue, at single-cell–level resolution. These last approaches preserve spatial context and provide insights into cellular organization, signaling pathways, and immune cell interactions that cannot be captured using bulk or dissociative methods alone.
By integrating mechanistic insights with innovative spatial technologies, this symposium aims to bridge biological discovery and methodological innovation. The session will foster interdisciplinary dialogue between neurobiologists, immunologists, and technology-driven researchers, while highlighting emerging directions for translational research aimed at modulating neuroinflammation for therapeutic benefit in brain injury and neurological disease.
12:30 Danilo De Gregorio
Neuropsychopharmacology Unit, Division of Neuroscience, IRCCS San Raffaele Hospital, Milan, Italy
"Psychedelics as Modulators of Neuroimmune Function"
Psychedelic compounds such as lysergic acid diethylamide (LSD) are gaining renewed interest as potential therapeutics in psychiatry. While their effects on neuroplasticity are well recognized, emerging evidence suggests that they also modulate immune function. Psychedelics acting at 5-HT2A receptors can regulate inflammatory responses, including the inhibition of pro-inflammatory cytokines and the modulation of immune cell activity . Recent studies further highlight the importance of neuroimmune interactions in shaping brain function and behavior .
In this talk, I will provide an overview of the immunomodulatory properties of psychedelics and discuss how these compounds may influence neuroimmune crosstalk. Preliminary preclinical observations will be presented to illustrate how psychedelics can impact microglial function, suggesting a role beyond classical anti-inflammatory effects, potentially linked to synaptic plasticity.
13:10 Marta Kamińska
Broegelmann Research Laboratory, Department of Clinical Science, Faculty of Medicine, University of Bergen, Bergen, Norway
"Infection-Specific Reprogramming of Microglia in Alzheimer's Disease"
Alzheimer’s disease (AD) is increasingly recognized as a disorder driven not only by protein aggregation but also by chronic neuroinflammation. While microglia are key regulators of this immune response, their heterogeneity - and how it is shaped by peripheral inflammatory triggers - remains incompletely understood.
Although oral pathogens have emerged as potential upstream contributors to neurodegeneration, their precise influence on microglial phenotypes has yet to be defined.
I will present a study in which we used a dual approach combining in vitro high-dimensional single-cell mass cytometry with in vivo imaging mass cytometry in a hTau-knock in 5xFAD mouse model to dissect how two major periodontopathogens - Porphyromonas gingivalis (Pg) and Tannerella forsythia (Tf) - reprogram microglial subpopulations.
We show that Pg, through its gingipains, drives transient but robust proinflammatory polarization of microglia, eroding regulatory subsets critical for lesion control, while Tf induces a more suppressive and potentially exhausted microglial profile. Importantly, these infection-specific phenotypes are recapitulated in vivo, where Pg infection causes depletion of mixed-activation microglia in the cortex and reshapes spatial interactions with amyloid/pTau-rich lesions.
This demonstrates that virulence factor–dependent reprogramming of microglia contributes to AD-relevant pathology in a region- and lesion-specific manner.
13:23 Julia Jarco
Wroclaw University of Science and Technology, Department of Chemical Biology and Bioimaging, Wroclaw, Poland; Institute for Biomedical Research of Barcelona (IIBB) - Spanish Research Council (CSIC), Department of Neuroscience and Experimental Therapeutics, Barcelona, Spain
"Type I Interferon Signalling Shapes Microglial Activation After Ischemic Brain Injury"
Ischemic stroke triggers a strong neuroinflammatory response involving resident microglia and infiltrating immune cells. Increasing evidence indicates that type I interferon (IFN-I)–related signaling pathways are activated in microglia following brain injury; however, the functional role of this response in shaping neuroimmune and immunometabolic processes remains unclear.
The aim of this study is to investigate the role of type I IFN signaling in microglial activation and immunometabolic responses following ischemic stroke, with particular focus on microglia–immune cell interactions within intact brain tissue.
A mouse model of ischemic stroke was used, including genetically modified mice with ablation of the type I IFN receptor (IFNAR-deficient mice). Immune cells were isolated from brain tissue and analyzed using imaging mass cytometry and flow cytometry to characterize microglial activation states and spatial interactions with infiltrating immune populations at single-cell resolution.
Preliminary analyses indicate that ischemic brain injury is associated with distinct microglial activation patterns linked to IFN-I signaling. Spatial profiling reveals heterogeneous microglial states and region-specific interactions with infiltrating immune cells, suggesting a potential role for IFN-I pathways in shaping the post-stroke neuroimmune microenvironment.
These findings provide insight into the involvement of type I IFN signaling in microglial immunometabolic responses after ischemic stroke. Spatially resolved approaches enable the identification of neuroimmune features that may be inaccessible to dissociative methods and contribute to a better understanding of post-injury neuroinflammation.
13:36 Alba Simats
Institute of Biomedical Research of Barcelona - Spanish National Research Council; Fundació Clínic per la Recerca Biomèdica-Institut d’Investigacions Biomèdiques August Pi i Sunyer
"Beyond the Brain: Systemic Immune and Cardiac Consequences of Stroke"
Immune responses play a central role in stroke pathology and recovery, with consequences that extend beyond neurological outcome. Rather than being limited to resident microglial responses, post-stroke inflammation reflects a brain–systemic immune axis in which peripheral immune cells and long-term systemic immune alterations also play a central role.
In this talk, I will present our recent work published in Cell, demonstrating that acute brain injury such as ischemic stroke further induces persistent epigenetic reprogramming of circulating innate immune cells, imprinting a peripheral innate memory state that might further compromise patient’s outcomes.
Using experimental stoke models and patient samples, we show that this transcriptional rewiring substantially increases susceptibility to secondary complications beyond neurological consequences, such as cardiac dysfunction.
Together, these findings position stroke as a systemic immunological disease and identify immune pathways as promising targets to improve long-term outcomes, acting in complement to immune mechanisms operating within the brain itself.
13:49 Diana Piotrowska
Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden
"Characterisation of Tau Pathology Differences between Brain Regions in Secondary and Primary Tauopathies Using Quantitative Mass Spectrometry"
Alzheimer’s disease (AD) is characterised by two major brain changes: plaques of the amyloid beta (Aβ) protein, and tau protein accumulations, i.e. tangles. However, tau protein can form aggregates also independently of Aβ in neurodegenerative diseases called primary tauopathies.
Tau profiles in soluble and insoluble fractions from postmortem brain samples of superior temporal gyrus (STG) and fusiform gyrus (FuG) from patients with primary age-related tauopathy (PART), corticobasal degeneration (CBD), progressive supranuclear palsy (PSP), intermediate and late-stage AD were compared to gain knowledge of tau pathological forms in these regions.
Tau from intermediate AD (int-AD, Braak III-IV, n=20), high-AD (Braak V-VI, n=20), CBD/PSP (n=10), and PART (n=12) cases was analysed. Soluble (tris-buffered saline, TBS) and sarkosyl-insoluble (SI) brain extracts were immunoprecipitated with the HT7 antibody. Tryptic peptides were monitored by liquid chromatography/high-resolution data-dependent mass spectrometry using isotope-labelled standards for quantification.
In the SI fraction, tau peptides’ levels were much increased in the high-AD group compared to PART in both analysed regions, and the difference was largest for the MTBR peptides. However, in the int-AD group, levels of the same peptides were increased in FuG but not in STG, where they resembled those of the PART and PSP/CBD groups. The phospho-peptides’ levels followed the MTBR peptide pattern. In the TBS fraction, the between-group differences were much less pronounced, apart from the phospho-peptides, which were much increased in the high-AD group.
The brain regional difference in abundance levels of the MTBR and phospho-tau peptides is clear in int-AD, but much less pronounced in high-AD, CBD/PSP, and PART, suggesting that FuG is affected earlier in the disease course. Low MTBR peptide accumulation in PART, despite the same Braak stage as int-AD, suggests that tau pathology in PART is much less pronounced.
Chairman: Julia Jarco
