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Life Sciences Center, Vilnius University, Lithuania
Dr. Urte Neniskyte received her PhD in Biochemistry at the University of Cambridge (UK) and contributing to the first studies that identified microglial phagocytosis of live neurons as a mechanism contributing to neurodegeneration. She then joined the group of Dr. Cornelius Gross at the Epigenetics and Neurobiology Unit of the European Molecular Biology Laboratory (EMBL), Italy for her post-doctoral fellowship funded by Marie Skłodowska Curie Actions (MSCA) to identify molecular signals that guide synaptic pruning by microglia. After returning to the Life Sciences Center of Vilnius University with another MSCA fellowship, U. Neniskyte established a Molecular Neurobiology research group. Since 2021 Urte is a group leader at Vilnius University and European Molecular Biology Laboratory Partnership Institute for Genome Editing Technologies. Dr. Neniskyte’s is currently investigating mechanisms that are required for the maturation of neuronal networks during brain development. The aberrations of these processes are associated with a range of neurodevelopmental disorders, such as autism spectrum disorder, schizophrenia or epilepsy. For her achievements, Urte has received multiple awards, including L’Oréal-UNESCO For Women in Science International Rising Talent award (2019) and Presidential award of Knight’s Cross of the Order of the Lithuanian Grand Duke Gediminas (2019). In addition to her scientific research, Urte participates at various policy-making groups, such as the State Progress Council of Lithuania, and actively communicates science to diverse audiences.
The overarching focus of this symposium is on the bidirectional communication between the brain and the periphery in brain health and disease. There is an increasing recognition of the concept that different peripheral pathways, ranging from gut microbiome, to metabolites, to extra-cellular vesicles can alter brain molecular signatures and functionality. Aberrations in brain-body interactions, especially due to environmental factors can alter the susceptibility and progression of several neuropsychiatric disorders. This symposium will cover several key themes under the umbrella of brain-body interactions; including a plenary lecture on immunometabolic basis of neurodevelopmental disorders (Urte Neniskyte, Vilnius University), and short talks on the mitigating potential of secondary bile acids on neuroinflammation (Edyta Bulanda, Nencki Institute) and interaction between peripheral lipids and microglia in resilience vs. susceptibility to the long-term behavioral effects of adverse childhood experiences (Weronika Tomaszewska, Nencki Institute).
Western diet today has excessive fat content, causing increased obesity rates in human population worldwide, including women of reproductive age. There is growing evidence that maternal high-fat diet (mHFD) increases the risk of neurodevelopmental disorders in the offspring. To investigate the pathways that mediate the effect of mHFD on offspring neurodevelopment, we set up mHFD model, in which female C57Bl/6J mice were fed a control diet (CD, 10% fat) or high-fat diet (HFD, 60% fat) from weaning to lactation and were mated with males maintained on normal diet. The offspring were weaned to normal diet. We investigated the phenotype of the offspring social interaction, cognitive function, repetitive behavior and in other behavioral tests. The changes of offspring brain structure were determined by high-resolution voxel-based morphometry. Structural analysis was supplemented by immunohistochemistry of brain tissue sections, while gut microbiota was determined by 16S amplicon sequencing. We found specific deficits in offspring social behaviors that were accompanied by the alterations in olfactory areas of the brain and microglial activation in olfactory bulb. The consumption of HFD changed the relative abundance of different gut bacteria genera in the dams and this dysbiosis was transferred to the offspring as well. Interestingly, observed changes were sex-dependent, as structural brain alterations were more prominent in males, while microbiota changes were more notable in female offspring. Overall our findings suggest that social deficits observed in mHFD models may stem from impaired olfactory interactions in parallel or together with the dysbalance of gut microbiota composition.
