Dr. Georges Lévesque received his B.Sc. in Biochemistry from the Université du Québec à Montréal (UQAM). He continued his studies at Laval University, where he obtained a certificate in pedagogy, a Master’s degree in medical biochemistry, and a Ph.D. in cellular and molecular biology. He then embarked on a postdoctoral fellowship on the molecular genetics of Alzheimer’s disease at the Centre for Research in Neurodegenerative Diseases at the University of Toronto. He is a co-discoverer of the presenilin 1 and 2 genes, along with their mutations that lead to the development of an early, familial form of Alzheimer’s disease. Dr. Lévesque received the first Frist-Jus Memorial Award for Neurodegenerative Disease Research from the University of Toronto. He joined Laval University in late 2001. He is currently Assistant Director and Full Professor in the Department of Psychiatry and Neuroscience of the Faculty of Medicine, and continues his basic research activities on Alzheimer’s disease within the neuroscience axis of the CHU de Québec.
Presenilin, amyloid and the genetics of Alzheimer’s disease;
Dr. Lévesque’s research interests focus on the molecular aspects of Alzheimer’s disease. This disease is characterized by the degeneration of the central nervous system. The biochemical mechanisms leading to Alzheimer’s disease are not fully known. His team is studying the biochemical pathways by which the mutated form of presenilin leads to the degeneration of nerve cells and an early and aggressive form of Alzheimer’s disease. Dr. Lévesque has shown that presenilin is partly responsible for amyloid peptide synthesis, the accumulation of which causes neuronal damage to Alzheimer’s patients. Presenilin mutations amplify amyloid levels. In parallel with the studies on the fundamental role of presenilin, and in order to counter amyloid peptide synthesis, Dr. Lévesque began developing a therapeutic molecule, a ribozyme, to reduce levels of amyloid precursor mRNA and in turn block the accumulation of this peptide, which is responsible for neuronal degeneration. Dr. Lévesque, in collaboration with Dr. Emmanuel Planel, is also interested in creating a ribozyme directed against Tau protein mRNA, which is responsible for neurofibrillary tangles associated with cognitive deficits in Alzheimer’s pathology. Dr. Lévesque is also studying the role of genetic markers associated with Alzheimer’s disease, identified via genome analysis of a French Canadian population.
The role of FUS protein in lateral amyotrophic sclerosis;
Most recently, Dr. Lévesque initiated a project on amyotrophic lateral sclerosis, aimed at recreating the FUS protein mutations responsible for this pathology in iPS cells, using CRISPR- Cas9 technology. These modified cells will be used to screen libraries of molecules that may interfere with the toxicity of the mutated FUS protein.
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FANCC localizes with UNC5A at neurite outgrowth and promotes neuritogenesis.Journal Article
BMC Res Notes, 11 (1), pp. 662, 2018.
Fanconi anemia core complex-dependent HES1 mono-ubiquitination regulates its transcriptional activity.Journal Article
BMC Res Notes, 11 (1), pp. 138, 2018.
The Fanconi anemia pathway has a dual function in Dickkopf-1 transcriptional repression.Journal Article
Proc Natl Acad Sci U S A, 111 (6), pp. 2152-7, 2014, ISSN: 0027-8424.
The Fanconi anemia group C protein interacts with uncoordinated 5A and delays apoptosis.Journal Article
PLoS ONE, 9 (3), pp. e92811, 2014.
Fanconi anemia proteins interact with CtBP1 and modulate the expression of the Wnt antagonist Dickkopf-1.Journal Article
Blood, 121 (10), pp. 1729-39, 2013, ISSN: 0006-4971.
Silencing of amyloid precursor protein expression using a new engineered delta ribozyme.Journal Article
Int J Alzheimers Dis, 2012 , pp. 947147, 2012.
Hypothermia-induced hyperphosphorylation: a new model to study tau kinase inhibitors.Journal Article
Sci Rep, 2 , pp. 480, 2012, ISSN: 2045-2322.
δ-Catenin is genetically and biologically associated with cortical cataract and future Alzheimer-related structural and functional brain changes.Journal Article
PLoS ONE, 7 (9), pp. e43728, 2012.
Identification of novel NPRAP/δ-catenin-interacting proteins and the direct association of NPRAP with dynamin 2.Journal Article
PLoS ONE, 6 (10), pp. e25379, 2011.
A nuclear function for the presenilin 1 neuronal partner NPRAP/δ-catenin.Journal Article
J Alzheimers Dis, 27 (2), pp. 307-16, 2011, ISSN: 1387-2877.
- 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
- Discovery of Therapeutic Targets for FUS-Dependant Forms of ALS., Subvention, Société canadienne de la sclérose latérale amyotrophique, Arthur J. Hudson translational team grant program-2015, from 2015-10-01 to 2020-09-30