Nadege Morisot

Nkarta’s differentiated cell therapy approach is designed to boost and enhance the inherent power of Natural Killer cells to target and destroy tumor cells

Within the Drug Discovery division at Charles River, I helped our clients selecting appropriate in vivo models and optimizing study protocols to fulfill the specific objectives of their thrilling research programs. I directed in vivo pharmacological, behavioral and PK/PD studies to evaluate the therapeutic potential of candidate drug compounds in preclinical models. Supporting our Neuroscience and Oncology service portfolio, I oversaw and administered in vivo microdialysis projects, which aimed at continuously measuring the extracellular concentration of molecules of interest (drug compound, proteins, antibodies...) in various tissues in freely moving rodents. In addition, I conducted scientific data analysis, interpretation and reporting. I also enjoyed supervising the biotechnical team of nine great research associates.

At UCSF, I led preclinical research on the brain mechanisms underlying alcohol addiction. In particular, I surveyed the activation of signaling molecules by excessive alcohol drinking within neuronal circuits. Using pharmacological agents, viral-mediated gene delivery and transgenic animal models, I modulated the activity of alcohol-associated signaling pathways and investigated the consequences on addiction-like behaviors. Over 3 years of exciting collaborative research, I found that specific brain molecules are crucial to the development of harmful and uncontrolled alcohol drinking. My work suggests that targeting these molecules is a potential strategy to treat people suffering from alcohol addiction.

During my time as a PhD student at Bordeaux University, I investigated the role of the brain stress-responsive system in drug addiction. Using a combination of molecular and behavioral approaches, I unraveled how the "stress" receptor, named CRF2, contributes to drugs of abuse-induced cognitive and social deficits in preclinical models. In particular, I showed that genetic deletion of CRF2 prevents the influence of stress on addiction-like phenotypes. My work suggests that CRF2 is a potential target to treat drug addiction. In addition to my own research project, I had the chance to supervise undergraduate students projects.

While I was completing my master's degree, the Institute of Research Servier gave me the immense opportunity to contribute to an exciting scientific project: studying the implication of the neurotransmitter glutamate in schizophrenia, a major psychiatric disorder. In particular, I tested the effect of glutamatergic agents in preclinical models recapitulating cardinal symptoms of the disease. The central findings of my study revealed that enhancement of the glutamate function via modulation of the brain receptor mGluR5 prevents deficits in social cognition which is a core cognitive domain impacted in schizophrenia.

PhD thesis titled "Corticotropin-releasing factor 2 receptor-deficiency reduces memory and social deficits induced by cocaine"

Neurosciences and Neuropsychopharmacology