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Claudia Bagni

Claudia Bagni, Department of Fundamental Neurosciences, University of Lausanne, Switzerland


Diversity of the post-synaptic density proteome and behavioral deficits in Fragile X syndrome


Claudia Bagni, Full Professor at the University of Lausanne & University of Rome Tor Vergata received her PhD in Cellular and Molecular Biology from the University of Rome Tor Vergata. After postdoctoral positions held at the CNRS in Toulouse, Harvard University in Cambridge and EMBL in Heidelberg, she established her laboratory as assistant then full professor at the University of Rome Tor Vergata, to continue as full professor and group leader at the K University of Leuven –VIB, Belgium. In 2016 she became the Director of the Department of Fundamental Neurosciences at the University of Lausanne and in 2021 the Vice-Dean of Research and Innovation at the University of Lausanne. Her laboratory has a long-lasting interest in the study of intellectual disabilities such as Fragile X Syndrome and Autism in which the recurring aspect is the dysregulation of the synaptic proteome. She is interested in examining molecular mechanisms at dysfunctional synapses to identify processes that govern impaired behaviors. Her laboratory uses mice, flies, human stem cells and organoids. She has received national and international awards: she is an EMBO member, received the UCB Award and the Solvay Price given by the Queen Elisabeth Medical Foundation for Neuroscience (BE), the Nestle Research & Development – Women in Science Award (CH). She is an honorary member of the Italian fragile X association (IT).             

Website: https://wwwfbm.unil.ch/dnf/group/cellular-and-molecular-studies-of-synaptic-plasticity-and-cancer-in-intellectual-disabilities


Fragile X syndrome (FXS) is a neurodevelopmental disorder caused by dysfunctions in the RNA binding protein FMRP (encoded by the FMR1 gene). Here we show how the specific composition of the post-synaptic density (PSD) across brain regions confers susceptibility to FXS. We demonstrate that altered protein composition in specific brain regions drives behavioral inflexibility, a typical feature of FXS individuals. We have identified the impaired molecular pathway and restored the behavioral deficits providing opportunities for the development of future strategies for the treatment of specific FXS traits