Dr. Andréa C. LeBlanc is a James McGill Professor in the Department of Neurology and Neurosurgery at McGill University and a researcher at the Bloomfield Center for Research in Aging at the Lady Davis Institute for Medical Research in Montreal. Dr. LeBlanc is also an Associate Member in the Department of Anatomy and Cell Biology and in the Division of Geriatric Medicine at McGill. She received a Ph.D from the Department of Biochemistry at Dalhousie University and did her post-doctoral training in the Department of Neurology at the Mayo Clinic and Mayo Foundation in Rochester, Minnesota. Dr. LeBlanc initiated her studies on Alzheimer and prion diseases as an assistant professor in the Department of Pathology at Case Western Reserve University in Cleveland from 1989 to 1993.
She is renowned for her discovery of Caspase-6 in early Alzheimer disease and her work on the neuroprotective function of normal cellular prion protein. The prion work was chosen as one of Quebec Science Top 10 discoveries in 2003. Dr. LeBlanc has been a member of several committees at the National Institutes of Health and was recently appointed to their College of Scientific Review. She has been a Chercheur boursier and a Chercheur national of the Fond de recherche en santé du Québec. In 2009, she was the first woman to receive an Honoris Causa Doctorate es Science from the University of Moncton.
Major Research Activities
Since 1993, Dr. LeBlanc has investigated the underlying molecular mechanisms responsible for the pathophysiology of neurodegenerative diseases in aging individuals. Using several molecular and cellular biology techniques, the research in her laboratory focuses on two neurodegenerative diseases: Alzheimer disease and prion diseases. In Alzheimer disease research, Dr. LeBlanc’s team studies cell death mechanisms in human primary neuron cultures. Her main research goal is to test the hypothesis that the degenerative events in human aged neurons are the leading physiological abnormality contributing to the loss of a critical mass of functional neurons in the central nervous system (CNS) and that this loss is the underlying cellular reason for the CNS deficit and the associated pathology in Alzheimer Disease. Recently, the team has identified intense Caspase-6 activity associated with early neurodegenerative events in age-related cognitive deficits and in Alzheimer disease and believes that Caspase-6 activation is a critical determinant of cognitive impairment and dementia in Alzheimer disease. Dr. LeBlanc also identified an anti-cell death function for the normal cellular form of prion protein and continues to investigate the regulation of prion protein expression, trafficking, and function in normal and pathological conditions. Recently, her team identified phosphorylation as a physiological mechanism for the conversion of the normal cellular prion protein into a disease-associated conformer.
LeBlanc AC, Ramcharitar J, Afonso V, Hamel E, Bennett DA, Pakavathkumar P, Albrecht S: Caspase-6 activity in the CA1 region of the hippocampus induces age-dependent memory impairment in mice and men. Cell Death and Differentiation,696-706, 2014.
Foveau, B, Beauchemin, N, Ursini-Siegel, J, LeBlanc, AC. Inflammation induced tumorigenesis in the colon is not dependent on Caspase-6 PLoS One 2014 Dec 3;9(12):e114270. doi: 10.1371/journal.pone.0114270.
Vikas Kaushal, Rebecca Dye, Bénédicte Foveau, Prateep Pakavathkumar, Bradley Hyman, Bernardino Ghetti,Beverly H. Koller, Andrea C. LeBlanc.Neuronal NLRP1 inflammasome activation of Caspase-1 coordinately regulates inflammatory interleukin-1-beta production and axonal degeneration-associated Caspase-6 activation.Cell Death Differ. 2015 22(10):1676-86. doi: 10.1038/cdd.2015.16.
Pakavathkumar P*,Sharma G*,Kaushal V, LeBlanc AC: Methylene blue inhibits the activity of Caspase-6. Scientific Report –2015 ;5:13730. doi: 10.1038* share first co-authorship
Peters S,MA Dery, LeBlanc AC: Familial prion protein mutants inhibit Hrd1-mediated retrotransmlocation of misfolded proteins. Human Molecular Genetics 2016 25(5):976-88. doi: 10.1093/hmg/ddv630.