Email: gary.armstrong [at] mcgill.ca (Gary Armstrong )
Recent Publications: Research gate, Google Scholar
Academic Affiliations: Assistant Professor, Department of Neurology and Neurosurgery
Research Groups: Rare Neurological Diseases, Neurodegenerative Diseases
“I’m particularly interested in what’s going wrong at the cellular level in the spinal cord of patients with ALS," says Armstrong. "The better we can understand defects that arise there, the quicker we can advance therapeutic discovery.”
Gary Armstrong is Assistant Professor in the Department of Neurology and Neurosurgery at the Montreal Neurological Institute and a Killam Scholar. His research focuses on furthering our understanding of synaptic defects arising both at peripheral neuromuscular junctions and central spinal cord synapses in the neurodegenerative disease Amyotrophic Lateral Sclerosis (ALS). To investigate these defects his research team uses zebrafish, an animal model uniquely suited for investigations (using electrophysiological, optogenetic, and imaging approaches) pertaining to synaptic function at all levels of the motor system. In addition, this animal model lends easily to genomic manipulations where analogous disease-associated mutations can be edited into zebrafish orthologs of human genes involved with ALS (e.g. TARDBP, FUS, CHCHD10, TBK1 and C9orf72) using the clustered regularly interspaced short palindromic repeats (CRISPRs) mutagenic system. These novel gene-edited animal models permit investigations of disease-causing variants in a native context e.g. similar expression levels and patterns as opposed to transgenic animal models that often rely upon transgene over-expression and non-endogenous promotors to confer a disease phenotype.
In addition to the fundamental research, the Armstrong laboratory is also involved in translational therapeutic drug discovery where his team is developing a zebrafish drug screening platform to bridge research findings made by scientists working with cellular models of neurodegenerative diseases with zebrafish models. This will enable validation of novel therapeutics in an animal model forming a critical step in advancing drug discovery.
Armstrong obtained his M.Sc. (2003-2005) and PhD (2005-2009) at Queen’s University, Kingston Ontario, where he studied adaptations that confer neuroprotection of circuit function during acute exposures to stress (hyperthermia/hypothermia and hypoxia/anoxia). His Postdoctoral research was carried out in the Department of Pathology and Cell Biology (2010-2014) at Université de Montréal and later in the Department of Neurosciences (2014-2016) at the CRCHUM in Montreal, Québec, where he conducted research examining synaptic defects in ALS zebrafish models.
Patten, S.A.*, Aggad, D.*, Martinez, J., Tremblay, E., Petrillo, J., Armstrong, G.A.B., La Fontaine, A., Maios, C., Liao, M., Ciura, S., Wen, X.-Y., Rafuse, V., Ichida, J., Zinman, L., Julien, J.-P., Kabashi, E., Robitaille, R., Korngut, L.**, Parker, J.A.**, Drapeau P**. Neuroleptics as therapeutic compounds stabilizing neuromuscular transmission in amyotrophic lateral sclerosis. JCI Insight. 2(22):e97152 (2017). * Co-first author. **Co-senior author.
Dzieciolowska, S., Drapeau, P., G.A.B. Armstrong. Augmented quantal release of acetylcholine at the vertebrate neuromuscular junction following tdp-43 depletion. PLoS ONE. 12(5): e0177005 (2017).
Armstrong, G.A.B.*, Liao, M.*, You, Z., Lissouba, A., Chen, B.E., Drapeau, P. Homology directed knockin of point mutations in the zebrafish tardbp and fus genes in ALS using the CRISPR/Cas9 system. PLoS ONE. 11(3): e0150188. (2016). * Co-first author
Armstrong, G.A.B., and Drapeau, P. Loss and gain of FUS function impair neuromuscular synaptic transmission in a genetic model of ALS. Human Molecular Genetics. 22:4282-4292 (2013).
Armstrong, G.A.B., and Drapeau, P. Calcium channel agonists protect against neuromuscular dysfunction in a genetic model of TDP-43 mutation in ALS. The Journal of Neuroscience. 33:1741-1752 (2013).
Rodgers-Garlick, C.I., Armstrong, G.A.B., and Robertson, R.M. Metabolic stress modulates motor patterning via AMP-activated protein kinase. The Journal of Neuroscience. 31:3207-3216 (2011).
Armstrong, G.A.B., López-Guerrero, J.J., Dawson-Scully, K.D., Peña, F., and Robertson, R.M. Inhibition of protein kinase G activity protects neonatal mouse respiratory network from hyperthermic and hypoxic stress. Brain Research. 1311:64-72 (2010).
Armstrong G.A.B., Rodgers C.I., Money T.G.A., and Robertson R.M. Suppression of spreading depression-like events in locusts by inhibition of the NO/cGMP/PKG pathway. The Journal of Neuroscience. 29:8225-8235 (2009).
Armstrong, G.A.B., Shoemaker, K.L., Money, T.G.A., and Robertson, R.M. Octopamine mediates thermal preconditioning of the locust ventilatory CPG via a cAMP/PKA signaling pathway. The Journal of Neuroscience. 26: 12118-12126 (2006).