o 2010- : Ass. Prof. (Chargé de Recherche 1), Inserm-Nantes University UMR 1064, CHU Hotel Dieu, Nantes. Neuroinflammation, estrogen, metabolism, multiple sclerosis.
o 2004-09: Ass. Prof. (Chargé de Recherche 1), Inserm-UPMC UMR 732 & 546, Paris. Chemokines, estrogen and neuroinflammation.
o 2002-03: Research Associate, Dept Neuroscience, University of Medecine and Dentistry of New Jersey, USA. Neuronal pathology in models of multiple sclerosis.
o 1997-2001: Research Associate, Dept Neuroscience and Cell Biology, University of Medecine and Dentistry of New Jersey, USA. Epigenetic control of neural precursor proliferation.
o 1995-96: Postdoctoral Fellow, Lab. Neurobiology and Behavior, Rockefeller University, NY, USA. In vivo antisense strategy, estrogens and behavior.
o 1993-95: Visitor, Medical Pharmacology/Center for Biopharmaceutical Sciences, Leiden, The Netherlands. Neurotensin antagonists & stress. Inserm-NWO exchange & Biomed 1 european program.
o 1991-94: PhD student, Inserm U339, Paris. Neurotensin systems and neuroendocrine functions.
My reseacrh covered two main research topics, with possible translational research for defining new therapeutical strategies of two types of central nervous system disorders. I performed studies aimed at defining the effects of two extracellular signals in the regulation of proliferation and differentiation of neural progenitors, in particular the granule cerebellar precursors. In physiological conditions, an orderly control of mitogenic and anti-mitotic signals, in concert with chemotactic cues, leads to the proper postnatal generation of the mature granule cell layer in the cerebellar cortex. In humans, loss of regulatory control of granule cerebellar progenitors leads to medulloblastoma, the most common malignant childhood brain tumour. Our work has especially described how the neuropeptide PACAP and the matricial protein CCN3/NOV promote the maturation of these precursors in vitro. I now studying central nervous system inflammation and neurodegeneration. We addressed the issues of neuronal damage and reactive astrogliosis in murine models of multiple sclerosis, an autoimmune disorder of the central nervous sytem, in which the myelin sheet and oligodendrocytes have been regarded as major primary targets by the immune system. Reevaluation of the pathological processes in animal models and imaging studies in humans now indicate the involvement of both neurons and astroglia in early pathology and progression to chronicity. With Dr S. Elkabes, we have evidenced the early dysregulation of neuronal gene expression in the spinal cord during experimental encephalomyelitis, in particular the decrease in the neuronal isoform of the plasma membrane Ca2+ pump, PMCA2 and its consequence on axonal damage and neurodegeneration. Our work addresses the issue of the pathogenic arm of reactive astrocytes which are now recognized as important players in amplifying neuroinflammation, damage of oligodendrocytes and axon loss, and how this astrocytic reactivity can be moderated by sex steroids. Current work further focuses on defining immunological targets in the context of multiple sclerosis as wel as reactive astrogliosis, with the goal to identify new strategies to favor CNS repair.