Public Lectures

2018 Public Lecture:

(This is a free lecture that takes place the evening before the main conference and it is open to the public. To RSVP your attendance, please email

Public Lecture 2018

Previous Public Lectures:

2017 Public Lecture:

Screen Shot 2018-06-19 at 9.31.54 AMDr. Dayan Goodenowe
President & CEO, Prodome Sciences

Dr. Goodenowe, research scientist, founded Prodrome Sciences Inc. to implement robust, clinical validation and implementation protocols for preventative therapeutics. Dr. Goodenowe is the inventor of numerous patents related to the diagnosis and treatment of neurodegenerative diseases, including those relating to plasmalogens, key regulators of cholesterol dynamics.

“I do not believe that disease is either random or unpredictable. However, medicine, as it is currently practiced, is based upon this passive acceptance model. Passive, in that we primarily wait for disease to happen to us, and accepting in that we assume that we are powerless, in any specific way, to predict or prevent a specific disease prior to its occurrence.”

2016 Public Lecture:

screen-shot-2017-02-09-at-11-06-44-amDr. Steffany Bennett, Ph.D.
Associate Director, Centre for Catalysis Research & Innovation
Professor/University Research Chair in Neurolipidomics/Neural Regeneration Laboratory (U of Ottawa)
“The Fatty Brain – Do we think what we eat? Brain lipids, 
cognition and neurodegenerative disease”

Dr. Steffany Bennett is a lipid biochemist and systems neurobiologist working to block the pathological changes in brain lipid metabolism that precipitate pediatric and geriatric neurodegenerative disease. She received her Ph.D in Biochemistry at the University of Ottawa and post-doctoral training at the W. Alton Cell Science Centre and Harvard Medical School.  She is a Full Professor and University Research Chair in the Department of Biochemistry, Microbiology, and Immunology, University of Ottawa.  Her team is developing and applying methodologies in super-resolution imaging (stimulated emission depletion STED), liquid chromatography electrospray ionization mass spectrometry (LC-ESI-MS), and bioinformatics to advance the emerging field of neurolipidomics.  Specifically, she focuses on identifying (a) circulating phospholipids and glycolipids at the molecular level that predict disease conversion, (b) how changes in these structural and second messenger lipids signal neurodegeneration, and (c) whether these changes can be targeted to resist neurodegenerative disease in the central nervous system.  As part of this lipidomics approach, her team explores how changes in membrane composition alter function of integral membrane connexin and pannexin channel in neurons, glia, and neural/glia progenitor populations with overarching goal of protecting neurons from excitotoxic insult and enhancing effective neuro- and glial regeneration.

2015 Public Lecture: Featured two speakers: 

Katherine Bick, Ph.D.

Katherine Bick, Ph.D.

Katherine Bick, Ph.D.
“How Senility became a Disease: The early years.”

Katherine Livingstone Bick was born in Clyde River, Prince Edward Island, attended school there and later Prince of Wales College in Charlottetown. She graduated from Acadia University with both an Honours degree in Biology and her M.Sc. Later she earned her doctorate in Biology from Brown University in Rhode Island. She has held faculty appointments at UCLA, Cal State Northridge CA, and Georgetown University. She received an honorary Doctor of Science from Acadia in 1990. Her involvement in the dementias began at the Neurology Institute at the National Institutes of Health in Bethesda MD where she was Deputy Director for some years. Later she was appointed  Deputy Director for Extramural Programs for the NIH. She has also participated in international studies of dementia with colleagues in Italy and through the World Health Organization. She has served as a consultant to Dana Foundation for research in neuroscience. She is the author/editor of several books on Alzheimer’s Disease, notably Alzheimer’s Disease: Senile Dementia and Related Disorders, considered a seminal publication for later studies. Her more recent book (with her long-time friend and colleague, Robert Katzman) is  Alzheimer Disease: The Changing View, which  provides a personal look at both the scientists and the families who led the efforts for increased research in the dementias.

Ben Wolozin, M.D., Ph.D. Boston University School of Medicine

Ben Wolozin, M.D., Ph.D.
Boston University School of Medicine

Benjamin Wolozin, M.D., Ph.D.
Boston University School of Medicine
“What causes Dementia & Parkinson’s Disease and what we can do about it?”

Dr. Wolozin is a professor in the Department of Pharmacology. The goal of his research is to understand the mechanisms underlying neurodegenerative diseases, and then to use this understanding to develop novel interventions for disease. Much of his research focuses on the central concept of regulated protein aggregation. Protein aggregation in neurodegenerative diseases is classically thought to occur as an unwanted byproduct of protein misfolding. Human genetic studies increasingly highlight the importance of RNA binding proteins in neurodegenerative diseases. This is important because RNA binding proteins use protein aggregation as part of a normal regulated, physiological mechanism controlling protein synthesis. Aggregated RNA binding proteins for stress granules, transport granules, P bodies, as well as participate in physiological functions, such as activity dependent protein synthesis.  Our research investigates the hypothesis that dysfunction of RNA granules causes neurodegenerative diseases.  Over active stress granule formation could contribute to neurodegeneration by altering patterns of protein synthesis and sequestering proteins that regulate cell death processes.  Hypo-active stress granules leads to inadequate neuroprotection.Dr. Wolozin has received numerous awards for his research including the Donald B. Lindsley Prize, Society for Neuroscience, the A. E. Bennett Award and a Merit Award from Alzforum. He serves on numerous editorial boards, including for the Journal of Biological Chemistry and Neurodegenerative Diseases, and is a standing member of the NIH CDIN study section.

2014 Public Lecture: 

ZigmondMichael Zigmond, Ph.D. (U. of Pittsburgh)
Returning to our Forebearers: How more exercise can lead to less neurodegeneration

Dr. Michael J. Zigmond is Professor of Neurology University of Pittsburgh. Over the past year, Dr. Zigmond and his research team have continued their studies of cellular and animal models to examine Parkinson’s disease (PD), which they believe is a multi-factorial disorder. A major focus of the lab is the role of intracellular signaling cascades in determining the viability of dopamine (DA) neurons. They hypothesize, for example, that trophic factors such as GDNF and oxidative stress can both stimulate intracellular survival cascades, including those involving MAP kinases. They further believe that endogenous trophic factor expression can be enhanced by exercise which in turn can be neuroprotective. And they have evidence that protection also can derive from acute exposure to low levels of a neurotoxin, a form of preconditioning. Last year their work included studies of the impact of oxidative stress induced by 6-hydroxydopamine (6-OHDA), a DA analogue that is concentrated in DA cells and rapidly breaks down to form reactive oxygen species. Results from these and other studies suggest that DA neurons react to stress by initiating a set of protective responses. Learning more about these responses may provide insights into new treatment modalities for PD. In the coming year, Dr. Zigmond will continue to focus on understanding the strategies DA neurons use to reduce their vulnerability to intracellular stress. For example, studies are underway to determine if inhibition of trophic actor action or of kinase activation will block neuroprotection seen with exercise or GDNF or increase 6-OHDA toxicity. Some of these studies involve the preparation of molecular biological tools that maintain kinases in a constitutively or dominant negative state and/or localize a kinase to the cytoplasm or the nucleus. In addition, histochemical methods are being developed to quantify kinase levels in different cellular compartments of identified cells. Dr. Zigmond also is involved in the influence of environmental enrichment on Parkinson’s Disease and age-related decline and working with decision scientists to try to understand why we make such poor decisions about our lifestyle.

2013 Public Lecture: 

M~ prv102199mcgeer-1Patrick McGeer, Ph.D. (UBC)
“How can you painting a health brain and avoid Dementia?”

Dr. McGeer graduated from University of British Columbia in 1948 with a first class honours in chemistry and then went on to Princeton for his Ph.D. (1951). After graduating from Princeton, McGeer went to work as a researcher at DuPont, where he met a fellow researcher, Edith Graef. They married in 1954 and returned to British Columbia, where he earned an M.D. in 1958, while Edith went to work at the Kinsmen Laboratory for Neurological Research in the Faculty of Medicine at UBC.In 1959, Pat joined Edith as a professor at the UBC Faculty of Medicine. The two of them rapidly became a formidable research team, building the Kinsmen Lab into a premier neurochemistry facility with a particular focus on the degenerative neurological diseases of aging. Although now officially retired, they both continue to research and publish in brain-related research, particularly on Alzheimer’s disease, Parkinson’s disease, ALS and multiple sclerosis, with more than 800 papers and three books. Their research in the study of the function of neurotransmitters in the brain has been pivotal to the pathology of Parkinson’s disease and Alzheimer’s disease. In 2002 they were jointly inducted as Fellows of the Royal Society of Canada, and in 2005 they were jointly inducted into the Order of British Columbia.