Seminar Series

This talk explores how hippocampal activity coordinates large-scale cortical networks during sleep and memory consolidation. Using multimodal imaging and electrophysiology, I will highlight how hippocampal outflow engages the default mode network, reorganizes cortical communication, and supports the reactivation of spatial information across the cortex.

Altered neuronal activity may precede irreversible neuron loss and overt symptoms in neurodegenerative diseases such as Alzheimer's and Huntington's disease. However, it is unclear if and how these early functional changes contribute to subsequent neurodegeneration. Dr. Mackay's research program combines genetic mouse models, in vivo imaging of brain activity and machine learning to test whether neuronal activity can predict disease development before behaviorally disease evidence emerges and to identify the cellular/molecular mechanisms underlying any such biosignatures. This work aims to uncover modifiable targets, establish their causal roles in neurodegeneration and ultimately inform development of novel therapeutics for human disease.

Dr. Mackay received a BSc in Pharmacy from the University of Alberta (2008) and his PhD in Pharmacology (2016) under Dr. William F. Colmers, investigating NPY signaling in the basolateral amygdala. He then completed a postdoc with Dr. Lynn A. Raymond at the University of British Columbia, studying aberrant glutamate signaling and sensory processing in Huntington disease. Dr. Mackay joined the University of Alberta, Department of Pharmacology as an assistant professor in 2025, his current research uses machine learning and advanced neuroimaging to identify early brain changes in neurodegenerative disease, with the goal of discovering early biomarkers and therapeutic targets.

Dr. Ruthazer will present multiphoton in vivo structural and functional imaging studies in the brains of translucent Xenopus tadpoles that reveal how astrocytes and microglia actively participate in the refinement and response selectivity of the developing visual system.

Edward Ruthazer is the James McGill Professor of Neurology and Neurology at the Montreal Neurological Institute in McGill University. Until last year he was the Director of the McGill Integrated Program in Neuroscience graduate program with nearly 600 MSc and PhD students.

Dementia is a growing burden in our aging population, and head injury earlier in life is a prominent risk factor. Dr. Allison's team has developed larval zebrafish as a model of traumatic brain injury, and use it to probe mechanisms leading to cell death and tauopathy. They observe seizures occur following injury, and that amplifying or reducing these seizures can increase or decrease neurodegenerative outcomes. They also find that modulating neuroinflammation can alter the course of seizures, and vice versa, suggesting a feed-forward mechanism of snowballing pathology shortly after injury. The data spotlights larval zebrafish as a bioethically-favourable entry point to understanding and treating neurotrauma. The work suggests that further efforts are warranted in discovery of pathomechanisms, including study of longer time courses and translating combinatorial treatments into rodent models.

Dr. Allison is a proud NMHI member, and a Professor in the Department of Biological Sciences at the University of Alberta, where he began in 2008. His PhD was completed at the University of Victoria with Professor Craig Hawryshyn. His PDF examined retinal development using zebrafish at U Michigan, Ann Arbor, with Collegiate Professor Pamela Raymond. His team primarily works with zebrafish, and sometimes other fishes, to understand neural system evolution, development and neurodegenerative conditions. Particular areas of focus are evolution of the retina, and appreciating the role of hyper-excited neurons in degenerative diseases including models of tauopathy and ALS.

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Dr Vande Velde will explore the role of the phase separated biocondensates known as stress granules and how they relate to TDP-43, and their contribution to neuronal loss that characterizes ALS pathogenesis. Her talk will leverage an in vivo stress paradigm and mouse models of TDP-43. She will also discuss the molecular mechanisms by which TDP-43 regulates the central stress granule assembly factor G3BP1.

Dr. Christine Vande Velde is Full Professor in the Department of Neurosciences at the Université de Montréal and Université de Montréal Hospital Research Center (CRCHUM). Her research is centered on understanding the underlying pathological mechanisms that lead to the fatal neurodegenerative diseases amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) and the exploitation of that knowledge for biomarker and therapeutic development. Dr. Vande Velde is the current Scientific Director of the Robert Packard Center for ALS Research at Johns Hopkins and a member of the Scientific and Medical Advisory Council of ALS Canada.