Hélène MarieInstitut de Pharmacologie Moléculaire et Cellulaire (IPMC) - CNRS / Université Côte d’Azur

Mes recherches

I studied Molecular Biology at the University of Edinburgh, Scotland.  I then obtained my PhD in Neuroscience in 2000 as a member of the 4 Year Welcome Trust PhD Program of the University College London, England under the supervision of Profs. David Attwell and Stephen Moss.  To perfect my skills in the electrophysiological analysis of synapse function, I spent four years (2001-2005) at Stanford University, USA, in the laboratory of Prof. Robert Malenka as a post-doctoral fellow, with an international prize from the Wellcome Trust.  In 2010, I started my independent career by heading my own research group as junior faculty at the European Brain Research Institute in Rome, Italy, an institute directed by the Nobel laureate Rita Levi-Montalcini. In 2010, after 18 years abroad, I decided to move back to France, my home country, and integrated the CNRS as CR1. For this integration, I benefited from the ATIP-AVENIR funds. I started my independent team at the Institute of Molecular and Cellular Pharmacology (IPMC) situated at the heart of Sophia-Antipolis. I became DR2 CNRS in 2017. By combining my strong pioneering expertise in in vivo viral mediated expression of recombinant proteins, patch clamp electrophysiology and analysis of rodent behavior, my current research group studies the molecular and cellular mechanisms of neuronal plasticity at the level of a single neuron and in the context of neuronal circuits. I have spearheaded the identification of new mechanisms driving neuronal plasticity and how these mechanisms become altered in the context of Alzheimer’s disease. Notably, I have recently reported how different peptides issued from the cleavage of the amyloid precursor protein (APP) regulate synapse function and intrinsic excitability (Willem et al. Nature 2015; Kootar et al. Neurobiology of Disease 2017; Pousinha et al. Elife 2017; Pousinha et al. Cell Reports 2019). This new information should help to unravel how the hippocampus becomes dysfunctional during Alzheimer’s disease progression.