Join us for our final seminar of 2024.
December 18, 4pm ET
Assistant Professor of Neuroscience, Veterinary Biomedical Sciences, University of Saskatchewan.
Bio:
Olamide is an Assistant Professor of Neuroscience at the University of Saskatchewan’s Department of Veterinary Biomedical Sciences. She holds a DVM and PhD from the University of Ibadan, Nigeria. She was a Fulbright Visiting Postdoctoral Fellow at Cornell University (2019), USA, and BrainsCAN Tier I postdoctoral fellow at Western University (2022-2024), London, ON.
Her research focuses on understanding how myelin integrity is disrupted in heavy metal-induced neurotoxicity and neurodegenerative diseases, to identify novel therapies for remyelination and repair. She has presented at international conferences, and received several awards, including the Young Investigator Education Enhancement Award from the American Society of Neurochemistry, and have numerous peer-reviewed publications.
She is an affiliate of the African Academy of Sciences, a representative for the IBRO Early Career Committee, and lead an advocacy group, Made4More, promoting neuroscience research among underrepresented groups.
Outside of work, she enjoys sightseeing, hiking, and traveling.
Abstract:
Myelin is the fatty substance that surrounds neurons and speeds up the transmission of electrical impulses. It is also critical to metabolic support and signal conduction in neurons. Oligodendrocytes are glial cells of the central nervous system essential for myelin synthesis. When myelin is damaged and not replaced by oligodendrocyte-producing cells, this results in demyelinating lesions around axons leading to neurodegeneration and impairments in sensory, motor, and cognitive functions. Currently, there is no cure for demyelinating diseases.
This talk will focus on the effects of Vanadium, a metal released during oil exploration and mining, on myelin integrity in various brain regions and its effects on cognition and motor functions. I will highlight the mechanisms behind this metal-induced myelin damage and introduce a novel approach using genetically modified proteins activated by synthetic drugs to stimulate repair.
Our findings identify factors that increase the risk of developing demyelinating and suggest that neuronal activity promotes remyelination by accelerating oligodendrocyte precursor cell proliferation and differentiation following demyelination.
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The CBSN/RCSN gratefully acknowledges the University of Toronto Scarborough and its support as the Network Host Institution, and the Academic Program Committee of the Network for the BE-STEMM Seminar Series.