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

2001- 2004: Post-doctoral position. Host laboratory: Prof. Rizzuto Rosario. University of Ferrara, Italy.

2004- 2005: Post-doctoral position. Host laboratory: INSERM U370 directed by Prof. Christian Bréchot, Paris V University, France.

2005-2008: INSERM young investigator contract. Host laboratory: INSERM U807, directed by Prof. Patrizia Paterlini Bréchot,Paris V University, France.

2009-2010: Team leader, Italian Institute of technology, Department of Neuroscience and Brain Technologies, directed by Prof. Fabio Benfenati, Genova, Italy

Since 2011: Researcher (CR1 INSERM), Institute of molecular and cellular pharmacology, team of Dr. Frédéric Checler, UMR 7275-CNRS, Nice-Sophia Antipolis University, Valbonne, France.

 Teaching activity

- Teaching of molecular biology and biochemistry (PCEM1) and of cellular biology (PCEM2), Paris V University, France.

- Teaching of Master 1 and Master 2 degrees, Paris V and XI Universities and Nice University, France.

- PhD Students Cycle Courses, Italian Institute of Technology, Genova, Italy.

Research supervision

Since 2001: Supervision of Master 1, Master 2 and PhD students.

Fellowships, patent and scientific prizes

2017: Grant from the Academy 4, IDEX University Côte d'Azur « Living systems Complexity and diversity », trans-disciplinary master project.

2014: LECMA (Ligue Européenne contre la maladie d'Alzheimer) grant.

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

2001: National PHD award « Association Nationale des Enseignants de Biologie Cellulaire ».

2004 : Post-doctoral fellowship Roux, Pasteur institute.

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

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

1998 : National PhD fellowship « la Ligue Nationale Contre le Cancer » and the « Fondation pour la Recherche Médicale ».

2000 : Patent « cellular genes implicated in oncogenesis, diagnostic and therapeutic applications ». INSERM patent N° 00 11 826, 2000.

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 and in a neuromuscular disease related to mitochondrial respiratory chain complex II deficiency. I also described a new truncated isoform of the calcium pump SERCA 1, called S1T. The S1T protein, induced by ER stress, is located in MAMs, thus promoting calcium leak from the ER to mitochondria and the induction of mitochondrial apoptosis. This knowledge in the field of calcium signalling, ER stress and mitochondrial pathology prompted me to study the role of calcium signalling 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 amyloide 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 deregulationof l)pif metabolism related to AD. Interestingly, we recently reported that the intracellular domain of APP (AICD) regulates the expression of Pink1, a key molecular marker for the elimination of defective mitochondria by mitophagy. These studies open the possibility of identifying new molecular targets for the treatment of AD.

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