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25.04.2026, Saturday, 10:00-11:30
The symposium explores interplay of brain immune cells, microglia, with metabolic cascades across the lifespan that shape vulnerability and resilience to metabolic, neurodevelopmental, and neuropsychiatric conditions. Microglia have quintessential roles in the central nervous system both in maintaining brain homeostasis but also during development and activity-dependent synaptic remodeling. Concrete research during the past two decades further reveals microglial involvement in nearly all neurodegenerative and neuroinflammatory diseases. Therefore, understanding the molecular processes that shift microglial states from adaptive to pathological has become a considerable priority in neuroscience. This symposium integrates multi-modality research efforts revealing the convergence of microglia and systemic metabolic factors to influence brain health- from prenatal development to aging. The symposium will kickstart with a leading discussion on sex-specific regulation of systemic metabolism in mice focused on combinatorial refinement of hypothalamic circuits by hormonal, neuronal, and immune cues. Extending this theme to early development, the second talk will examine how maternal perinatal metabolic insults in mice alter retinal microglia and Müller cells in the offspring. The third talk will discuss ongoing translational studies in humans demonstrating how adverse childhood experiences shape adult mental health via lipid-mediated microglial signaling. The symposium will conclude with a discussion on the mediating role of microglial metabolism in driving synaptic loss in neurodegenerative disorders. Together, these perspectives will highlight the intricate relationship between systemic influences and microglia dynamics in determining brain and metabolic health. Furthermore, by elucidating the factors that shift microglia toward protective or pathological states, molecular cascades that are amenable to enhance resilience against brain and metabolic diseases will be brought to focus.
University of Bordeaux, INSERM, Neurocentre Magendie, Bordeaux, France
"Role of brain immunity in the regulation of metabolism"
Across evolution, female mammals have developed exceptional metabolic flexibility. Hormonal and innate genetic factors enable them to sustain reproduction during periods of food scarcity and efficiently allocate energy while supporting energetically demanding fetuses. This evolutionary advantage gives females a remarkable capacity to maintain energy balance under a wide range of physiological conditions, from handling a calorie-rich meal to withstanding fasting. Central to this regulation is the hypothalamus, which integrates hormonal, neuronal, and nutritional cues. Within this structure, diverse cell populations interact to precisely coordinate whole-body metabolism, including food intake and energy expenditure. Our research aims to uncover the neuroimmune mechanisms that underlie the heightened metabolic resilience seen in females. In my presentation, I will share data demonstrating how microglia and a subpopulation of lymphocytes collaborate to regulate hypothalamus activity and related metabolic function.
Institute of Biosciences, Life Sciences Center, Vilnius University, Lithuania
"The effect of maternal high-fat diet on the peripheral retina of the offspring"
Obesity and high-fat diets are increasingly being recognized as major drivers of global disease burden. Critically, their impact on health begins even before birth. Our research explores how maternal high-fat diet (mHFD) influences retinal development in offspring, revealing surprising sex-specific effects. Using C57Bl/6J mice, we examined microglial activation and Müller cell changes in the peripheral retina, focusing on biomarkers CD68, TSPO, and GFAP. While mHFD reduced microglial area in males, it increased it in females hinting at hormonal modulation during the estrous cycle. These subtle yet significant alterations suggest that reproductive hormones may shape retinal inflammatory responses, adding a new dimension to neurodevelopmental risk factors. This talk will highlight how diet, immunity, and sex hormones intersect in shaping the development of visual system health and their potential role in modulating neurodevelopment disease risk.
Łukasiewicz Research Network- PORT Polish Center for Technology Development, Wroclaw, Poland
"Decoding Resilience: How Lipid Signals and Microglia Shape Outcomes After Adverse Childhood Experiences"
Why do some individuals thrive despite adverse childhood experiences (ACE), while others develop neuropsychiatric disorders? Our work explores the biological underpinnings of this resilience–vulnerability spectrum, focusing on peripheral metabolic factors and microglial function. Using human microglia-like cells (HMC3), iPSC-derived microglia, and serum from ethnically diverse ACE cohorts, we discovered that serum from ACE-susceptible individuals disrupts microglial metabolism and synaptoneurosome phagocytosis. Transcriptomic analysis points to altered glucose metabolism as a key driver. Intriguingly, transfection with miR-142-3p—a microRNA differentially expressed in resilient vs. susceptible serum—mimicked these effects, identifying it as a potential molecular mediator. This talk will highlight how lipid-mediated signals and microglial responses converge to influence mental health trajectories, opening new avenues for biomarker discovery and targeted interventions.
Faculty of Medicine, Medical University of Warsaw, Warsaw, Poland
"Microglial Hyperactivation in TDP-43 ALS: Metabolic Drivers of Synaptic Phagocytosis"
This presentation will examine the interplay between metabolic and immunological mechanisms driving the progression of amyotrophic lateral sclerosis (ALS) associated with TDP-43 mutations. Although research has traditionally focused on motor neurons as the primary cells affected in ALS, emerging evidence indicates that dysregulated microglial activity plays a substantial role in disease progression. The talk will focus on integrated transcriptomic, metabolomic and phenotypic analyses performed in TDP-43 knockdown murine (BV2) and human (HMC3) microglial cells, modelling the loss of this essential RNA/DNA-binding protein in vivo. It will discuss how alterations in metabolic pathways and gene expression may contribute to an overall hyperphagocytic phenotype, as well as the excessive clearance of both pathogenic and non-pathogenic cargo. Finally, the presentation will highlight current knowledge gaps and consider how new experimental platforms may support deeper mechanistic insight and facilitate the translation of these findings towards therapeutic interventions.
[Affiliation]
"Differences in the metabolic profiles of brain lesions in radiologically isolated syndrome and clinically definite multiple sclerosis revealed by MR spectroscopy"
[Abstract]
