Dr. Dorian Sargent earned a doctor of pharmacy degree and an M.S. in molecular and cellular infectiology from the Philippe Maupas University of Tours followed by a Ph.D. in neuroscience from the Claude Bernard University of Lyon in France, which allowed him to develop dual skills in vectorology and neuroscience. During his Ph.D., his research focused on Parkinson’s disease, describing how does the aggregation of α-synuclein, the main component of Lewy bodies found in the brain of patients with Parkinson’s, can propagate in a transgenic mouse model. He also tested a new gene therapy strategy against the aggregation of α-synuclein in mice and worked on the development of new models of Parkinson’s disease using viral vectors carrying human α-synuclein gene. In November 2018 he joined the laboratory of Dr. Darren Moore at Van Andel Institute as a postdoctoral fellow.
The D620N mutation of vacuolar protein sorting 35 ortholog (VPS35) has been associated with familial cases of Parkinson’s disease. VPS35 protein is a subunit of a protein complex called the retromer, which is located in endosomes, and participates in the recycling of transmembrane proteins’ cargo, and facilitates the transport of these proteins from the endosome to the plasma membrane or from the endosome to the Golgi complex. Since its discovery, the D620N mutation of VPS35 has also been associated with neurodegeneration in various animal models of Parkinson’s disease, but the mechanisms leading to this degeneration remain unclear. The goal of this project is to explore and describe these mechanisms using different animal models, including a knock-in mice model expressing mouse VPS35 mutated in D620N at physiological levels. We will focus on the potential interaction between VPS35 and leucine-rich repeat kinase 2 (LRRK2), another protein known as the greatest genetic contributor to Parkinson’s disease, and the role that LRRK2 might play in the development of the disease.
Ph.D. in neuroscience, Claude Bernard University of Lyon (Advisor: Dr. Thierry Baron, Dr. Dominique Bétemps)
Thesis: Molecular study of the propagation of the aggregation of α-synuclein in a transgenic model of Parkinson’s disease: impact of the overexpression of β-synuclein mediated by adeno-associated vectors (AAV)
Pharm.D. in molecular and cellular infectiology, Philippe Maupas University of Tours
M.S. in molecular and cellular infectiology, Philippe Maupas University of Tours
Neuroscience Congress in Bordeaux
Sargent D et al., 2017. Adeno-associated virus vector-mediated overexpression of β-synuclein can have noxious effects on the M83 mice synucleinopathy.
Best poster prize, Journée des doctorants de l’ANSES
Sargent D et al., 2015. Propagation of the aggregation of α-synuclein in a transgenic model of Parkinson’s disease: development of a strategy to overexpress β-synuclein using adeno-associated virus vector (AAV).
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Sargent D, Betemps D, Drouyer M, Verchere J, Gaillard D, Arsac JN, Lakhdar L, Salvetti A, Baron T 2018. Investigating the neuroprotective effect of AAV-mediated β-synuclein overexpression in a transgenic model of synucleinopathy. Sci Rep.
Sargent D, Verchére J, Lazizzera C, Gaillard D, Lakhdar L, Streichenberger N, Morignat E, Betemps D, Baron T. 2017. “Prion-like” propagation of the synucleinopathy of M83 transgenic mice depends on the mouse genotype and type of inoculum. J Neurochem 143(1):126–135.
Sargent D, Baron T. 2016. Assemblies of alpha-synuclein: do different strains exist? Med Sci (Paris) 32(3):233–236.