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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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.
The H50Q mutation enhances α-synuclein aggregation, secretion, and toxicity.Journal Article
J Biol Chem, 289 (32), pp. 21856-76, 2014, ISSN: 0021-9258.
c-Abl phosphorylates α-synuclein and regulates its degradation: implication for α-synuclein clearance and contribution to the pathogenesis of Parkinson's disease.Journal Article
Hum Mol Genet, 23 (11), pp. 2858-79, 2014, ISSN: 0964-6906.
Polo-like kinase 2 regulates selective autophagic α-synuclein clearance and suppresses its toxicity in vivo.Journal Article
Proc Natl Acad Sci U S A, 110 (41), pp. E3945-54, 2013, ISSN: 0027-8424.
The many faces of α-synuclein: from structure and toxicity to therapeutic target.Journal Article
Nat Rev Neurosci, 14 (1), pp. 38-48, 2013, ISSN: 1471-003X.
Mimicking phosphorylation at serine 87 inhibits the aggregation of human α-synuclein and protects against its toxicity in a rat model of Parkinson's disease.Journal Article
J Neurosci, 32 (5), pp. 1536-44, 2012, ISSN: 0270-6474.
Phosphorylation at S87 is enhanced in synucleinopathies, inhibits alpha-synuclein oligomerization, and influences synuclein-membrane interactions.Journal Article
J Neurosci, 30 (9), pp. 3184-98, 2010, ISSN: 0270-6474.
Phosphorylation of synucleins by members of the Polo-like kinase family.Journal Article
J Biol Chem, 285 (4), pp. 2807-22, 2010, ISSN: 0021-9258.
Role of post-translational modifications in modulating the structure, function and toxicity of alpha-synuclein: implications for Parkinson's disease pathogenesis and therapies.Journal Article
Prog Brain Res, 183 , pp. 115-45, 2010, ISSN: 0079-6123.
Different functional basal ganglia subcircuits associated with anti-akinetic and dyskinesiogenic effects of antiparkinsonian therapies.Journal Article
Neurobiol Dis, 36 (1), pp. 116-25, 2009, ISSN: 0969-9961.
- 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