Ternational College for Advanced Research of Trieste, Varese, Italy; bCNR Institute of Neuroscience, Milano, Italy; cCNR Institute of Materials, Trieste, Italy; dInternational College for Sophisticated Research of Trieste, Trieste, Italy; eCNR Institute of Neuroscience, Trieste, Italyamanipulation, single MVs in suspension have been trapped by an infra-red laser collimated in to the optical path on the microscope, and delivered to neuron surface. The MV-neuron dynamics have been monitored by collecting bright-field photos. Results: Evaluation of time-lapse recordings revealed that MVs effectively adhered to neurons and about 70 showed a displacement along the surface of neurites. Interestingly, the MVs velocity (143 nm/sec) is in the similar array of retrograde actin flow, which regulates membrane diffusion of receptors linked to actin. Accordingly, we identified that MV movement is highly dependent on neuron power metabolism. Indeed, only 33 of MVs were capable to move on power depleted neurons treated with rotenone. Moreover, inhibiting neuron actin cytoskeleton rearrangements (polymerization and depolymerization) with cytochalasin D, which binds speedy increasing end of actin, the percentage of EVs able to move on neuron surface was drastically lowered from 79 to 54 , revealing that CD1c Proteins Synonyms neuronal actin cytoskeleton is involved in EV-neuron dynamics. Unexpectedly, we identified by cryo-electron microscopy that a subpopulation of MVs consists of actin filaments, suggesting an intrinsic capacity of MVs to move. To address this hypothesis, we inhibited actin rearrangements in EVs with Cytochalasin D and observed a significant decrease, from 71 to 45 , of MVs in a position to drift on neuron surface. Summary/Conclusion: Our data assistance two different way of MV motion. Within the initially case, MV displacement could be driven by the binding with neuronal receptors linked for the actin cytoskeleton. Inside the second, actin rearrangements inside MVs could drive the motion along a gradient of molecules on neuron surface.OF16.P2RX7 Inhibitor suppresses tau pathology and improves hippocampal memory function in tauopathy mouse model Seiko Ikezu, Zhi Ruan, Jean Christophe Delpech, Mina Botros, Alicia Van Enoo, Srinidhi Venkatesan Kalavai, Katherine Wang, Lawrence Hu and Tsuneya Ikezu Boston University College of Medicine, Boston, USAIntroduction: Microvesicles (MVs) play an essential role in intercellular communication. Exposing adhesion receptors, they’re able to interact with target cells and deliver complex signals. It has been shown that MVs also cover a vital function within the spreading of pathogens in neurodegenerative issues, but pretty much absolutely nothing is recognized about how MVs can transport messages moving within the extracellular microenvironment exploiting neuronal connections. Methods: So as to investigate the interaction of MVs with the plasma membrane of neurons, MVs released from cultured astrocytes and isolated by differential centrifugation, had been added to the medium of cultured hippocampal neurons. Utilizing opticalIntroduction: Microglia, the innate immune cells inside the central nervous technique, could spread pathogenic tau protein through secretion of extracellular vesicles, like exosome. P2X7 receptor (P2RX7) is an ATP-gated cation channel and highly expressed in microglia and triggers CD151 Proteins Purity & Documentation exosome secretion. We hypothesize that P2RX7 inhibitor could alleviate tauopathy in PS19 tau transgenic mice by inhibiting the exosome secretion by microglia.ISEV2019 ABSTRACT BOOKMethods: BV-2 murine microglial cell lines were treated w.