I earned a first-class honours degree in Biochemistry from the University of Sussex (UK) and a PhD in Biochemistry at Imperial College, University of London. I completed postdoctoral training at the University of California San Francisco. My lab is interested in advancing the understanding of neurodegenerative processes through molecular studies of the prion protein, APP and Tau and the creation of animal model resources. I was one of the original discoverers of the chromosomal gene encoding PrPC in 1985 and since then my lab defined the glycoproteins encoded by the paralogous genes known as Doppel and Shadoo. My co-workers and I also were part of the team that first revealed the physiological connection between the cellular prion protein PrPC and copper. Concerning Alzheimer’s disease, my post-doctoral fellow Azhar Chishti created the TgCRND8 rapid-onset mouse model of Alzheimer amyloidosis used around the world, and with Dr. Chris Janus, used it in a first demonstration of in vivo efficacy of Aβ-directed therapy on behavioural endpoints. With the same team my lab created TgTau(P301L)23027 mice with florid 4-repeat tauopathy (in neurons, glia and oligodendrocytes), neuronal loss and behavioural impairment. Recent analyses of these mice reveal unexpected diversity in their performance despite a congenic genetic background, indicating the impact of environmental influences or stochastic chemical events; these mice are a starting point for a new series of studies.
Dr. David Westaway was recruited to Alberta in 2006 to lead the development of prion research in the province. He trained with two Nobel laureates at the University of California in San Francisco. With foundational contributions to the molecular biology and animal modeling of neurodegenerative diseases he is one of Alberta’s highest impact scientists, with over 27,000 citations of his publications.
Leadership and Collaborations:
Dr. Westaway is professor in the Department of Medicine’s Division of Neurology and a member of the University of Alberta's Neuroscience and Mental Health Institute (NMHI). He is director of the Centre for Prions & Prion Folding Diseases. He is a member of the Canadian Consortium on Neurodegeneration in Aging and an advisory board member for the Canadian Institutes of Health Research’s Institute of Aging.
Dr. Westaway’s identification of the infective properties of the prion protein led to a new avenue of research: that of the involvement of prion-like mechanisms in human diseases. His subsequent discovery of specific proteins involved in prion diseases showed that interactions between different types of prion proteins lead to disease transmission in animals and humans. He developed models of early-onset Alzheimer’s disease for laboratory use. Dr. Westaway’s research spans genetic and molecular agents involved in neurological disorders in humans, including a current focus on tau proteins that, when misfolded, can cause dementias and Alzheimer’s disease.
Dr. Westaway’s research is funded through many provincial and national agencies including the former Alberta Heritage Foundation for Medical Research, the Canadian Institutes of Health Research, the Alberta Prion Research Institute and the Alzheimer’s Association (USA). He has published more than 180 articles in peer-reviewed journals; he has a h-index of 72 and an i10 index of 171.
Dr. Westaway’s research has received many awards including the Canadian Institute of Health Research Investigator Award, the Zenith Scholar Award from the Alzheimer’s Association (USA), the Dr. Don Rix Memorial Prion Mentorship Award from the PrioNet Network Centre of Excellence and the Premier’s Research Excellence Award from Ontario. He is a Tier 1 Canada Research Chair and a Fellow of the Canadian Academy of Health Sciences.
Alzheimer’s disease, amyloid, gene editing, histopathology, molecular biology, neurodegeneration, neuroscience, prion diseases, tau, transgenics
Knockout of the PrP-like Sprn gene does not produce embryonic lethality in combination with PrPC-deficiency.
Author(s): Daude, N. , Wohlgemuth, S. , Pitstick, R. , Gapeshina, . , Carlson, G. A. , Westaway, D.
Journal: PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES USA (E-pub)
Year: May 12, 2012
Prion disease tempo determined by host-dependent substrate reduction.
Author(s): Mays C. E. , Kim C. , Haldiman T. , van der Merwe J. , Lau A. , Yang J. , Grams J. , Di Bari M. A. , Nonno R. , Telling G. C. , Kong Q. , Langeveld J. , McKenzie D. , Westaway D. , Safar J. G.
Journal: J CLIB INVEST. (E-pub)
Year: Jan. 16, 2014 Jan 16.
Octarepeat region flexibility impacts prion function, endoproteolysis and disease manifestation.
Author(s): Lau A. , McDonald A. , Daude N. , Mays C. E. , Walter E. , Wohlgemuth S. , Yang J. , Shi B. , van der Merwe J. , Gapeshina H. , Kim C. , Grams J. , Wille H. , Balachandran A. , Schmitt-Ulms G. , Safar J. , Millhauser G. , Westaway D.
Journal: EMBO MOL. MED.
The CNS in inbred transgenic models of 4-repeat Tauopathy develops consistent tau seeding capacity yet focal and diverse patterns of protein deposition.
Author(s): Eskandari-Sedighi G. , Daude N., Gapeshina H. , Sanders D. W. , Kamali-Jamil R. , Yang J. , Shi B. , Wille H. , Ghetti B. , Diamond M. I. , Janus C. , Westaway D.
Journal: MOLECULAR NEURODEGNERATION
A novel Gerstmann-Sträussler-Scheinker disease mutation defines a precursor for amyloidogenic 8 kDa PrP fragments and reveals N-terminal structural changes shared by other GSS alleles.
Author(s): Mercer R. C. C. , Daude N. , Dorosh L. , Fu Z. L. , Mays C. E. , Gapeshina H. , Wohlgemuth S. L. , Acevedo-Morantes C. Y. , Yang J. , Cashman N. R. , Coulthart M. B. , Pearson D. M. , Joseph J. T. , Wille H., Safar J. G. , Jansen G. H. , Stepanova M. , Sykes B. D. , Westaway D.
Journal: PLOS PATHOG. (eCollection)
Year: Jan 2018