I gained my BSc degree in Biology at the University of Parma, where I became fascinated by neuroscience during an internship in the lab of Prof. Vittorio Gallese, studying self-disturbance in schizophrenia. Then, the University of Trieste and the International School for Advanced Studies (SISSA) offered me a multidisciplinary training in both basic and applied neurobiology so that in two years I gained my International MSc degree in Neuroscience. For my MSc thesis, I spent one year in Oxford, at the Department of Physiology, Anatomy, and Genetic (DPAG) in the group of Prof. Mike Glitsch and at The John Radcliffe Hospital in the group of Prof. Alastair Buchan, working on human brain vascular pericytes and their response to alteration in extracellular pH. Afterward, I moved to Sweden where I worked in the group of Prof. Christer Betsholtz at the Uppsala University's Rudbeck Laboratory. During my experience with Prof. Betsholtz, I worked on brain vascular pericyte physiology in two different mice models.
In 2017, I decided to start my DPhil and I came back to Oxford at DPAG and join the Ion Channels and Disease Initiative (OXION) funded by the Wellcome Trust. I started investigating the mechanosensing properties of a proton-sensing G-coupled receptor, under the mentorship of Prof. Glitsch, and then experienced the study of neuronal activity in Drosophila, under the supervision of Prof. Gero Miesenboeck. What fascinated me the most was the potential of visualizing and controlling the activity of a neuronal network, and subsequently the behavior, working on the expression of particular ion channels in the cells of interests. Currently, I am studying sleep homeostasis, focusing on chronic two-photon imaging of neuronal activity in Drosophila, in the group of Prof. Miesenboeck.
Adult-induced genetic ablation distinguishes PDGFB roles in blood-brain barrier maintenance and development
Vazquez-Liebanas E. et al, (2021), Journal of Cerebral Blood Flow & Metabolism, 0271678X2110563 - 0271678X2110563
Prolonged systemic hyperglycemia does not cause pericyte loss and permeability at the mouse blood-brain barrier.
Mäe MA. et al, (2018), Sci Rep, 8