Killam Seminar Series:Mechanisms of Multiple System Atrophy and Parkinson’s
Event Information
About this Event
Supported by the generosity of the Killam Trusts , The Neuro’s Killam Seminar series hosts outstanding guest speakers whose research is of interest to the scientific community at The Neuro and McGill University.
Speaker: Nadia Stefanova, MD, PhD, DSc
Professor of Translational Neurodegeneration Research, Medical University of Innsbruck, EU
Bio: Nadia Stefanova received her medical degree from the Medical University of Sofia, Bulgaria and the University of Innsbruck, Austria. She went on to complete a PhD in Neuroscience. Dr. Stefanova joined the Department of Neurology in Innsbruck where she performed her post-doctoral studies in Experimental Neurology, became Assistant Professor in 2006 and Associate Professor in 2011. Dr. Stefanova leads the Laboratory for Translational Neurodegeneration Research at the Department of Neurology, Medical University of Innsbruck. In April 2020 she was appointed full professor. Dr. Stefanova’s research focuses on the development and characterization of experimental models of multiple system atrophy and there utilization in target development and preclinical therapeutic screening. The MSA devoted studies of Dr. Stefanova address the implication of ectopic oligodendroglial aggregation of alpha-synuclein and neuroinflammatory responses in mechanisms that compromise neuronal viability in MSA.
Talk Title: "Mechanisms of Multiple System Atrophy and Other Parkinson’s Related Disorders"
Talk Abstract: Multiple system atrophy (MSA) is a rare late-onset neurodegenerative disorder characterized by α-synuclein inclusions in oligodendrocytes. The disease has a rapid progression with death of the patients within 6 to 9 years after the first clinical diagnosis and no effective cure. The causes of MSA remain largely unknown. Different animal models are applied to understand the disease mechanisms and identify targets for disease modification. Currently, experimental therapies focus on lowering the α-synuclein pathology and the neuroinflammation accompanying the neurodegeneration in MSA.
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