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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+1 418-525-4444, extension 49119
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Latest news

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Bartl S, Xie Y, Potluri N, Kesineni R, Hencak K, Cengio LD, Balazs K, Oueslati A, Parth M, Salhat N, Siddu A, Smrzka O, Cicchetti F, Staffler G, Hayden MR, Southwell AL

Corrigendum to "Reducing huntingtin by immunotherapy delays disease progression in a mouse model of Huntington disease" [Neurobiology of Disease, 2024 Jan:190:106376]

Journal Article

Neurobiol Dis, 193 , 2024.

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Bartl S, Xie Y, Potluri N, Kesineni R, Hencak K, Cengio LD, Balazs K, Oueslati A, Parth M, Salhat N, Siddu A, Smrzka O, Cicchetti F, Straffler G, Hayden MR, Southwell AL

Reducing huntingtin by immunotherapy delays disease progression in a mouse model of Huntington disease

Journal Article

Neurobiol Dis, 190 , 2024.

Abstract | Links:

Martínez-Drudis L, Bérard M, Musiol D, Rivest S, Oueslati A

Pharmacological inhibition of PLK2 kinase activity mitigates cognitive decline but aggravates APP pathology in a sex-dependent manner in APP/PS1 mouse model of Alzheimer's disease

Journal Article

Heliyon, 10 (20), 2024.

Abstract | Links:

Bérard M, Martínez-Drudis L, Sheta R, El-Agnaf OMA, Oueslati A

Non-invasive systemic viral delivery of human alpha-synuclein mimics selective and progressive neuropathology of Parkinson's disease in rodent brains

Journal Article

Mol Neurodegener, 18 (1), 2023.

Abstract | Links:

Teixeira M, Sheta R, Idi W, Oueslati A

Optogenetic-mediated induction and monitoring of α-synuclein aggregation in cellular models of Parkinson's disease

Journal Article

STAR Protoc, 4 (4), 2023.

Abstract | Links:

Lurette O, Martín-Jiménez R, Khan M, Sheta R, Jean S, Schofield M, Teixeira M, Rodriguez-Aller R, Perron I, Oueslati A, Hebert-Chatelain E

Aggregation of alpha-synuclein disrupts mitochondrial metabolism and induce mitophagy via cardiolipin externalization

Journal Article

Cell Death Dis, 14 (11), 2023.

Abstract | Links:

Sheta R, Teixeira M, Idi W, Oueslati A

Optimized protocol for the generation of functional human induced-pluripotent-stem-cell-derived dopaminergic neurons

Journal Article

STAR Protoc, 4 (3), 2023.

Abstract | Links:

Martínez-Drudis L, Sheta R, Pellegrinato R, Loukili S, Tremblay C, Calon F, Rivest S, Oueslati A

Inhibition of PLK2 activity affects APP and tau pathology and improves synaptic content in a sex-dependent manner in a 3xTg mouse model of Alzheimer's disease

Journal Article

Neurobiol Dis, 172 , 2022.

Abstract | Links:

Bérard M, Sheta R, Malvaut S, Rodriguez-Aller R, Teixeira M, Idi W, Turmel R, Alpaugh M, Dubois M, Dahmene M, Salesse C, Lamontagne-Proulx J, St-Pierre MK, Tavassoly O, Luo W, Del Cid-Pellitero E, Qazi R, Jeong JW, Durcan TM, Vallières L, Tremblay ME, Soulet D, Lévesque M, Cicchetti F, Fon EA, Saghatelyan A, Oueslati A

A light-inducible protein clustering system for in vivo analysis of α-synuclein aggregation in Parkinson disease

Journal Article

PLoS Biol, 20 (3), 2022.

Abstract | Links:

Sheta R, Teixeira M, Idi W, Pierre M, de Rus Jacquet A, Emond V, Zorca CE, Vanderperre B, Durcan TM, Fon EA, Calon F, Chahine M, Oueslati A

Combining NGN2 programming and dopaminergic patterning for a rapid and efficient generation of hiPSC-derived midbrain neurons

Journal Article

Sci Rep, 12 (1), 2022.

Abstract | Links:

35 entries « ‹ 1 of 4 › »
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Active projects

  • Deciphering the physiological role of alpha-synuclein aggregation in the central nervous system, from 2023-04-01 to 2028-03-31
  • Exploring the synergistic role of alpha-synuclein and tau in Alzheimer’s disease pathogenesis, from 2023-10-01 to 2026-09-30
  • Investigation of the synergistic role of TMEM106B and alpha-synuclein in Parkinson’s disease pathogenesis, from 2023-08-01 to 2025-01-31

Recently finished projects

  • Effects of post-translational modifications on intracellular alpha-synuclein oligomerization, from 2023-02-01 to 2024-07-31
  • Implication de l’alpha-synucléine dans la pathogenèse et les traitements de la maladie de Parkinson, from 2020-07-01 to 2024-06-30
  • Investigation of the synergistic role of PLK2 and alpha-synuclein in the regulation of neuronal homeostasis and functions., from 2016-04-01 to 2023-03-31
  • Unveiling the role of alpha-synuclein clustering and Lewy body formation in Parkinson’s disease pathogenesis using an optogenetic-mediated protein aggregation system, from 2019-04-01 to 2024-03-31
  • Use of optogenetic-TDP43 to shed light on the dying-back hypothesis in ALS, from 2022-04-01 to 2023-09-30
Data provided by the Université Laval research projects registery