MOUNIA CHAMI PhD-HDR

Course and current status

Education

2001:   PhD in molecular and cellular biology. Paris XI University, France. Host laboratory: INSERM U370, Faculty of Medicine Necker-Enfants malades. Paris V University, France.

2006: Diploma for research direction (HDR). Paris V University, France.

2007: Diploma for animal experimentation, level 1. Veterinary school, Lyon, France.

Work Experience

Since 2011: Research associate (permanent position, INSERM).  Institute of Molecular and Cellular Pharmacology (IPMC), CNRS UMR-7275, Valbonne, Sophia-Antipolis, France.

2009-2010: Team leader. The Italian Institute of technology, neuroscience and brain technologies department, Genoa, Italy.

2005-2008: INSERM young investigator contract. INSERM U807, Paris V University, Paris, France.

Teaching and mentoring experience

Teaching of molecular biology and biochemistry (PCEM1: first year of medicine), and of cellular biology (PCEM2: second year of medicine), Paris V University, France.

Teaching of Master 1 and Master 2 degrees, Paris XI University, France, and the Italian Institute of Technology, Genoa, Italy.

2019: Member of the reviewing committee for PhD Ministry fellowship (ED85)

Since 2014: Member of PhD and HDR reviewing committee (Caen Normandie University, and Paris VI University. France, and Sidi Mohammed Ben Abdellah University, Fez, Morocco).

2015: Nominated Mentor at INSERM.

2015: Member of the reviewing committee Polytechnic school, option “genie biology” (GB2), Sophia Antipolis.

Since 2011: Member of the reviewing committee of Master 1 et 2, Nice University Côte d’Azur.

2014: Member of the reviewing committee for Research associate n°66 MCF-1704, Lille University.

Research direction

Since 2011: CNRS UMR-7275_Principal investigator_ Research project: Endoplasmic reticulum signaling and of mitochondrial structure and function alterations in Alzheimer disease.

2009-2010: The Italian Institute of technology_Principal investigator_ Research project: Role of calcium signaling in Alzheimer Disease.

2005-2008: INSERM U807, Paris V University_Principal investigator_Research project: Physiopathology of Endoplasmic Reticulum stress and mitochondrial dysfunction.

Since 2008: Supervision of 7 PhD students (3 ongoing), 8 M.Sc. students, 4 research technicians, and 2 post-doctoral fellows (1 ongoing).

Ad hoc reviewer

Grants: Alzheimer association, FWO, Canadian Institut of Health Res, IIT project SEED, Fondazione Cassa di Risparmio di Padova e Rovigo.

Research articles: Cell death and disease, Journal of cell physiology, FASEB, Current Alzheimer research, J. neuroscience, Brain Behavior and immunity, Genes, J. Cell physiology, Mol. Neurodegeneration, Plos One, Scientific Reports, European Journal of Neuroscience, behavioral Brain Research, Autophagy, J. of Alzheimer Disease, Frontiers in Molecular Neuroscience, Cells.

2017: Associate Editor of Journal of Alzheimer Disease.

Honors

2006: Poster Award of the European Calcium Society (ECS).

2004: Post-doctoral fellowship Roux, Pasteur institute.

2002: Long term post-doctoral fellowship from the European Molecular Biology Organization (EMBO).

2001: National Ph.D. Award of the « Association Nationale des Enseignants de Biologie Cellulaire ».

2001: Post-doctoral fellowship Award from the «Association pour la Recherche sur le Cancer».

1998: National Ph.D. Fellowship Awards from «la Ligue Nationale Contre le Cancer» and «Fondation pour la Recherche Médicale».

Research Support

2019-2021: Grant from Fondation Vaincre la Maladie d’Alzheimer. PI.

2017-2018: Trans-disciplinary master project, IDEX-UCA-JEDI “Living systems Complexity and diversity”. Co-PI.

2013-2016: Grant from LECMA : Ligue européenne contre la maladie d’Alzheimer/Fondation Vaincre la Maladie d’Alzheimer. PI.

2008-2011: Grant from Fondation pour la Recherche Médicale. Co-PI.

2005-2008: Grant from Association Française contre les myopathies. Co- PI.

Scientific summary

My work has shown the role of calcium signalling deregulation in apoptotic cell death. I have highlighted the role of the contact sites between the endoplasmic reticulum (ER) and the mitochondria known also as MAMs (mitochondria-associated membranes) in the control of apoptosis, mitochondrial respiratory chain deficiency and of ER stress response. In this context, I described a new truncated isoform of the calcium pump SERCA 1, called S1T, induced by ER stress, located in MAMs, thus promoting calcium leak from the ER to mitochondria and the induction of mitochondrial apoptosis. This knowledge prompted me to study the role of calcium signaling deregulation and ER-mitochondria communication in the pathogenesis of Alzheimer's disease (AD). The recently obtained results demonstrate the impact of ER calcium homeostasis and specifically the role of the ryanodine receptor (RyR2) in amyloid precursor protein (APP) metabolism and the production of amyloid beta peptides, and in the development of cognitive deficits and synaptic plasticity dysfunction related to AD. These studies reveal RyR2 as a major molecular determinant in the development and/or progression of AD. Pharmacologic stabilization of RyR2 could be considered as a new therapeutic strategy for AD. My working hypothesis also postulate that the ER-mitochondria contact sites are deregulated in AD, favoring mitochondrial pathology associated with the disease development. Indeed, we have demonstrated the localization and metabolism of APP in MAMs and described the protein interaction of APP and its metabolites in this cellular microdomain. These results also reveal the potential involvement of impaired MAMs function in the deregulation of lipid metabolism related to AD. These results may open the possibility of identifying new molecular targets for the treatment of AD.

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