Résumés / Abstracts
Optogenetic-mediated spatiotemporal control of α-synuclein aggregation mimics authentic Lewy body formation and triggers neurodegeneration
MORGAN BERARD1,2, Razan Sheta1,2, Sarah Malvaut3,4, Raquel Rodriguez-Aller1,2,3, Maxime Teixeira1,2, Roxanne Turmel1,2, Melanie Alpaugh1,4, Marilyn Dubois1,2, Manel Dahmene1,2, Charleen Sales3,4, Jérôme Lamontagne-Proulx1,5, Marie-Kim St-Pierre1,2, Omid Tavassoly6, Wen Luo6, Raza Qazi7, Jae-Woong Jeong7,8, Thomas M. Durcan6, Luc Vallières1,2, Marie-Eve Tremblay1,2,9, Denis Soulet1,5, Martin Lévesque3,4, Francesca Cicchetti1,4, Edward A. Fon6, Armen Saghatelyan3,4, Abid Oueslati1,2
1CHU de Quebec Research Center, Axe Neurosciences. 2Department of Molecular Medicine, Faculty of medicine, Université Laval, Quebec City, Canada.3CERVO Brain Research Centre. 4Department of Psychiatry and Neurosciences, Faculty of medicine, Université Laval, Quebec City. 5Faculty of Pharmacy, Université Laval, Quebec City, Canada. 6McGill Parkinson Program and Neurodegenerative Diseases Group, Montreal Neurological Institute, McGill University, Montreal, Canada. 7Department of Electrical, Computer, and Energy Engineering, University of Colorado, Boulder, CO 80309, USA. 8School of Electrical Engineering Korea Advanced Institute of Science and Technology, Daejeon, 34141, Republic of Korea. 8Division of Medical Sciences, University of Victoria, Victoria, Canada.
α-synuclein (α-syn) aggregation into insoluble deposits, referred to as Lewy bodies (LBs) is the paramount pathological hallmark of Parkinson’s disease (PD) and related α-synucleinopathies. However, how these aggregates affect neuronal homeostasis leading to neurodegeneration remains elusive. This gap in knowledge is mainly due to the lack of proper cellular and animal models to undertake such investigations.