Scientist Profiles G-L

Michael F. Jackson, Ph.D.

Appointments & Affiliations

Associate Professor
Department of Pharmacology and Therapeutics
Rady Faculty of Health Sciences - Max Rady College of Medicine
University of Manitoba

Principal Investigator
Neuroscience Research Program, Winnipeg Health Sciences Centre

Research Information

Cellular and Molecular Neuroscience, Neurodegenerative diseases or disorders, Signalling molecules and pathways, Synaptic structure and organization, Glia-Neuron interactions

Michael Jackson joined the Department of Pharmacology & Therapeutics at the University of Manitoba in 2013. His laboratory is located at the Prairie Neuroscience Research Centre in the Kleysen Institute for Advanced Medicine (KIAM). Dr. Jackson obtained his PhD from McGill University in the Department of Pharmacology. Following postdoctoral training at the University of Toronto in the Department of Physiology, he moved to the Robarts Research Institute at Western University in 2008 as a Research Scientist and Adjunct Professor in the Department of Physiology and Pharmacology.

Expanded Summary
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Accumulation of soluble amyloid beta oligomers (AβOs) is closely linked to cognitive decline in Alzheimer’s disease (AD). Our research is focused on identifying molecular mechanisms through which AβOs disrupt the function and plasticity of glutamate excitatory synapses and thus precipitate cognitive decline. AβOs are known to provoke accumulation of glutamate, associated with excitotoxic stimulation of Ca2+ permeable NMDA-type glutamate receptors (NMDARs). Notably, partial block of NMDARs is responsible for the beneficial (though modest) response in patients treated with memantine/Ebixa, a “weak” NMDAR blocker. As more potent NMDAR blockers are associated with intolerable side effects, our research seeks to identify downstream effectors of NMDAR-initiated excitotoxic cascades. To this end, our research has identified distinct signalling cascades that link NMDARs to the activation of Ca2+ permeable non-selective cation channels TRPM2 and Pannexin 1 (Panx1). Moreover, AβO accumulation stimulates their aberrant activation, which in turn contributes to amyloid-induced impairment of synaptic transmission and plasticity. An extension of this work seeks to identify the consequence of aberrant TRPM2 and Panx1 activity 1) in synaptic compartments vulnerable to injury in neurodegeneration as well as 2) in microglia, a cellular compartment in which altered channel activation may stimulate synaptotoxic responses.


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