Dr. Oueslati is an Assistant Professor in the Department of Molecular Medicine at Laval University, Director of the Molecular and Cellular Neurodegeneration Laboratory at the CHU Research Center in Quebec City, and a member of the management committee of l’Axe de Neurosciences-CHUL.
Dr. Oueslati obtained his Advanced Studies Diploma (ASD) in Neurobiology (2004), as well as his Doctorate in neuroscience (2008) at the Université de la Méditerranée Aix-Marseille – Faculté des Sciences de Luminy, Marseille-France. He then joined The Brain and Mind Institute at l’École Polytechnique Fédérale de Lausanne (EPFL), Switzerland, for a Postdoctoral fellowship in the group of Dr. Hilal A. Lashuel (2008-2014). After a short experience in the pharmaceutical industry at the ‘EPFL Innovation Parc’, he joined Laval University as Associate Professor (2014), and then as Assistant Professor in June 2015.
The research program developed by Dr. Oueslati and his colleagues aims to understand the involvement of protein misfolding and aggregation in neurodegenerative diseases, including Parkinson’s and Alzheimer’s disease.
More specifically, Dr. Oueslati’s group are developing two lines of research:
- Role of post-translational modifications in the regulation of aggregation and protein toxicity in neurodegenerative diseases. The goal of this line of research is to understand how chemical modifications (e.g. phosphorylation) affect the aggregation and toxicity of certain proteins in the brain, including alpha-synuclein protein in Parkinson’s disease, and tau and amyloid beta proteins in Alzheimer’s disease. The results of this project will allow, on the one hand to identify new markers for the early detection of neurodegenerative diseases, and on the other hand, they will allow to develop new therapeutic targets for these crippling diseases.
- Role of prion propagation in the initiation and progression of neurodegenerative diseases. The goal of this project is to investigate how proteins involved in neurodegenerative diseases are able to spread from one neuron to another, and from one region of the brain to another, like prion disease. This spread of pathogenic proteins appears to play an important role in the initiation and progression of Parkinson’s disease and related diseases. The dissection of the molecular and cellular bases of this pathological propagation will allow to develop new therapeutic approaches that aim at stopping, or at least slowing, the progression of these neurodegenerative diseases.
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Use of adeno-associated virus-mediated delivery of mutant huntingtin to study the spreading capacity of the protein in mice and non-human primates.Journal Article
Neurobiol Dis, 141 , pp. 104951, 2020, ISSN: 0969-9961.
Evidence for the spread of human-derived mutant huntingtin protein in mice and non-human primates.Journal Article
Neurobiol Dis, 141 , pp. 104941, 2020, ISSN: 0969-9961.
Inhibiting cellular uptake of mutant huntingtin using a monoclonal antibody: Implications for the treatment of Huntington's disease.Journal Article
Neurobiol Dis, 141 , pp. 104943, 2020, ISSN: 0969-9961.
Dissecting the Molecular Pathway Involved in PLK2 Kinase-mediated α-Synuclein-selective Autophagic Degradation.Journal Article
J Biol Chem, 292 (9), pp. 3919-3928, 2017, ISSN: 0021-9258.
Induction of de novo α-synuclein fibrillization in a neuronal model for Parkinson's disease.Journal Article
Proc Natl Acad Sci U S A, 113 (7), pp. E912-21, 2016, ISSN: 0027-8424.
Implication of Alpha-Synuclein Phosphorylation at S129 in Synucleinopathies: What Have We Learned in the Last Decade?Journal Article
J Parkinsons Dis, 6 (1), pp. 39-51, 2016, ISSN: 1877-7171.
Human-to-mouse prion-like propagation of mutant huntingtin protein.Journal Article
Acta Neuropathol, 132 (4), pp. 577-92, 2016, ISSN: 0001-6322.
Parkinson disease mutant E46K enhances α-synuclein phosphorylation in mammalian cell lines, in yeast, and in vivo.Journal Article
J Biol Chem, 290 (15), pp. 9412-27, 2015, ISSN: 0021-9258.
Photobiomodulation Suppresses Alpha-Synuclein-Induced Toxicity in an AAV-Based Rat Genetic Model of Parkinson's Disease.Journal Article
PLoS ONE, 10 (10), pp. e0140880, 2015.
Protein Transmission, Seeding and Degradation: Key Steps for α-Synuclein Prion-Like Propagation.Journal Article
Exp Neurobiol, 23 (4), pp. 324-36, 2014, ISSN: 1226-2560.
- Centre de recherche du CHU de Québec - Université Laval, Subvention, Centre hospitalier universitaire de Québec - Université Laval, Centres de recherche affiliés, from 2017-01-01 to 2099-12-31
- Centre thématique de recherche en neurosciences, Subvention, Institutionnel - BDR, BDR - Centres de recherche reconnus, from 1999-06-01 to 2023-05-01
- Investigation of the synergistic role of PLK2 and alpha-synuclein in the regulation of neuronal homeostasis and functions., Subvention, Conseil de recherches en sciences naturelles et génie Canada, Subventions à la découverte SD (individuelles et d'équipe), from 2016-04-01 to 2021-03-31
- Unveiling the role of alpha-synuclein clustering and Lewy body formation in Parkinson’s disease pathogenesis using an optogenetic-mediated protein aggregation system, Subvention, Instituts de recherche en santé du Canada, Subvention Projet, from 2019-04-01 to 2024-03-31
Recently finished projects
- Clinicopathological Investigations of the substantia nigra in Parkinson's disease, Subvention, Parkinson Canada, Pilot Project Grant, from 2017-07-01 to 2019-06-30
- Implication de l’alpha-synucléine dans la pathogenèse et les traitements de la maladie de Parkinson, Subvention, Fonds de recherche du Québec - Santé, Établissement de jeunes chercheurs - Juniors 1, from 2016-07-01 to 2019-06-30
- Implication de l’alpha-synucléine dans la pathogenèse et les traitements de la maladie de Parkinson., Subvention, Fonds de recherche du Québec - Santé, Chercheur-boursier Juniors 1 et 2, Seniors, from 2016-07-01 to 2020-06-30
- Implication of Polo-like kinases in Alzheimer Disease pathogenesis and treatments, Subvention, Société Alzheimer du Canada, Subventions de recherche, from 2017-04-01 to 2020-03-31