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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Cell membrane expression of cardiac sodium channel Na(v)1.5 is modulated by alpha-actinin-2 interactionJournal Article
Biochemistry, 49 (1), 2010.
The fanconi anemia core complex acts as a transcriptional co-regulator in hairy enhancer of split 1 signalingJournal Article
J Biol Chem, 284 (20), 2009.
HES1 is a novel interactor of the Fanconi anemia core complexJournal Article
Blood, 112 (5), 2008.
Dissociated phenotypes in presenilin transgenic mice define functionally distinct gamma-secretasesJournal Article
Proc Natl Acad Sci U S A, 102 (25), 2005.
Presence and active synthesis of the 67 kDa elastin-receptor in human circulating white blood cellsJournal Article
Biochem Biophys Res Commun, 332 (3), 2005.
Regulation of the Fanconi anemia group C protein through proteolytic modificationJournal Article
J Biol Chem, 279 (6), 2004.
Presenilin-1 interacts directly with the beta-site amyloid protein precursor cleaving enzyme (BACE1)Journal Article
Neurobiol Dis, 13 (3), 2003.
Oligomerization of human presenilin-1 fragmentsJournal Article
FEBS Lett, 550 (1-3), 2003.
Presenilin-1 is indirectly implicated in Notch1 cleavageJournal Article
Neuroreport, 14 (12), 2003.
Dimerization of presenilin-1 in vivo: suggestion of novel regulatory mechanisms leading to higher order complexesJournal Article
Biochem Biophys Res Commun, 301 (1), 2003.
- The amyloid and beyond; A molecular answer to forget me not., from 2013-01-01 to 2024-03-31