After completing my undergraduate studies in biology at the University of Ottawa (Canada), I earned my MSc and PhD degrees at the Biozentrum in Basel (Switzerland), under the mentorship of Yves-Alain Barde. During my PhD, I investigated the instructive functions of neurotrophin tyrosine kinase (Trk) receptors and found that two of them, TrkA and TrkC, act as dependence receptors, providing a new understanding for long-standing questions in developmental neurobiology.
Funded by a long-term postdoctoral EMBO fellowship, I then joined the group of Nektarios Tavernarakis at the IMBB (Greece). My postdoc work investigated the molecular mechanisms underlying the phenomenon of hormesis in the nervous system, combining C. elegans and mouse genetics.
During my postdoc, I developed a strong interest in understanding the interplay between synaptic function and metabolic pathways. Autophagy is a conserved catabolic pathway which degrades macromolecules and defective or superfluous organelles by delivering them to the lysosome. Genetic studies have indicated that autophagy is indispensable for neuronal function. However, the mechanisms regulating autophagy in neurons remain poorly understood. With the support of a Marie Curie Career-Restart grant my first contribution to this niche revealed that Brain Derived Neurotrophic Factor (BDNF), a master regulator of synaptic plasticity, suppresses autophagy in the adult brain. Moreover, suppression of autophagy is necessary for BDNF-induced long-term potentiation (LTP) of synaptic strength and memory formation.
In 2017, I obtained an ERC starting grant and established my lab at the IMBB (Greece). The question we are asking is “how does autophagy contribute to synaptic function?”
The main goal of my lab is to study the role of autophagy in neural networks and animal behavior. Therefore, a major undertaking is to understand how degradation, secretion and targeting of proteins via autophagic intermediates contributes to different forms of plasticity, including long-term plasticity and homeostatic scaling. Converging evidence supports a pivotal role for these neural processes in cognitive functions that demand behavioral flexibility and their impairment is strongly implicated in autism spectrum and other neurodevelopmental synaptopathies. Understanding how autophagy operates in different neuronal populations to shape their synaptic networks and determine a behavioral outcome can lead to novel interventions for reversing behavioral deficits associated with these disorders. Moreover, my lab aims to characterize the synaptic cargo of autophagosomes in different neuronal populations and understand the molecular mechanisms underlying cargo selectivity. Towards these goals, we have gained expertise in cell and molecular biology tools, in vivo delivery of lentiviral vectors, confocal and electron microscopy and behavioral tests. In addition, we have developed unique biochemical techniques to isolate and purify autophagic vesicles from the mouse brain and cultured neurons and analyze their content using proteomic approaches.