ePoster · Neuroscience
Diego Julian Vesga Jimenez, Eugenia Vivi, Celia Román, Lea Seeholzer, Rachel Breton, Nathalie Rouach, Inga. D Neumann, Barbara Di Benedetto · FENS Forum 2024
Major Depressive Disorder (MDD) is a prevalent global cause of disability, affecting approximately 5% of adults, and has a higher incidence in females. Despite its significant impact, its diverse symptoms and causes lack clear identification, hindering effective treatments. Understanding the underlying mechanisms is crucial. Studies in various brain areas indicate an astrocyte pathology in MDD, revealing reduced numbers and altered morphology, gene, and protein expression. Astrocytes influence synapse remodeling, crucial for neuronal network maturation. Notably, their phagocytic ability, facil
ePoster · Neuroscience
Marie Denise Roggan, Sophie Crux, Felix Nebeling, Fabrizio Musacchio, Stefanie Poll, Juliane Schiweck, Manuel Mittag, Julia Steffen, Andrea Baral, Yvonne Schleehuber, Frank Bradke, Walter Witke, Martin Fuhrmann · FENS Forum 2024
Microglia, the immune cells of the central nervous system, are important for tissue homeostasis and in response to disease. Additionally, they are crucial during brain development, promote synapse elimination and survival, thereby even contributing to higher brain functions like cognition. Microglia are highly motile cells that continuously survey the brain parenchyma by extending and retracting their fine processes, yet the molecular mechanisms governing their dynamic shape changes are not fully understood.The cytoskeletal proteins actin depolymerizing factor and cofilin 1 (ADF/Cfl1) have est
ePoster · Neuroscience
Shinheun Kim, Woojin Won, Gyu Hyun Kim, Yeon Hee Kook, Mingu Gordon Park, Dong Yeop Kang, Young-Jin Choi, Kea Joo Lee, C. Justin Lee, Sangkyu Lee · FENS Forum 2024
The brain function is modulated by both rapid electrochemical activity of neurons and slow structural remodeling of synapses. Despite remarkable progress in controlling neural activity, methods for structural modulation of synaptic connections are still scarce. Here, we present a synthetic approach for synapse elimination via engineering of direct neuro-glial interactions which result in the uptake of synaptic components by astrocytes. The size-dependent synapse elimination in the CA3-CA1 circuit leads to a decline in synaptic connectivity, while the remaining synapses undergo reorganization o