Our research program is multi- and inter-disciplinary and focused on 3 overarching questions about Parkinson's disease:
What causes Parkinson's? Our Centre participates in studies on genetic causes of PD. Through our partnership with TRIUMF, we use positron emission tomography (PET) to study the natural history of dopamine cell loss in Parkinson's, mechanisms that the brain uses to compensate for this loss and the evolution of other neurochemical changes and pathological processes. We have a particular interest in studying populations at high risk of developing PD.
What mechanisms contribute to the complications of longstanding PD and its treatment? We have several projects related to this and while we have in the past focused on motor complications such as fluctuations in motor function and dyskinesias, we are now focusing on non-motor complications of PD, particularly depression, cognitive decline and impulse control disorders.
How can we use PD as a model to better understand the role of dopamine in the normal brain? We have a particular interest in the role of dopamine in signaling reward and its relevance to depression, impulse control problems and the placebo effect. We have shown that the placebo effect in PD is mediated by dopamine release and suggested that this likely contributed to placebo effects in other conditions as well.
CIHR, Michael J. Fox Foundation, Pacific Parkinsonís Research Institute, Weston Brain Institute.
Tier 1 Canada Research Chair (since 2000)
Member, Order of Canada (admitted 2007)
Fellow, Canadian Academy of Health Sciences (2009)
Co-Chair, World Parkinson Congress (since 2011)
Deputy Editor, Movement Disorders
de la Fuente-Fernandez R, Ruth TJ, Sossi V, Schulzer M, Calne DB, Stoessl AJ (2001). Expectation and Dopamine Release: Mechanism of the Placebo Effect in Parkinsonís Disease. Science 293: 1164-1166.
de la Fuente-Fernandez R, Sossi V, Huang Z, Furtado S, Lu J-Q, Calne DB, Ruth TJ, Stoessl AJ (2004). Levodopa-induced changes in synaptic dopamine levels increase with progression of Parkinson's disease: implications for dyskinesias. Brain 127: 2747-2754.
Adams JR, van Netten H, Schulzer M, Mak E, McKenzie J, Strongosky A, Sossi V, Ruth TJ, Lee CS, Farrer M, Gasser T, Uitti RJ, Calne DB, Wszolek ZK, Stoessl AJ (2005). PET in LRRK2 mutations: comparison to sporadic Parkinsonís disease and evidence for presymptomatic compensation. Brain 128:2777-85.† (subject of Editorial same issue).
Sossi V, de la Fuente-Fernandez R, Schulzer M, Troiano A, Ruth TJ, Stoessl AJ (2007). Dopamine transporter relation to dopamine turnover in Parkinson disease: a PET study. Annals of Neurology 62: 468-475.
Nandhagopal R, Mak E, Schulzer M, McKenzie J, McCormick S, Sossi V, Ruth TJ, Strongosky A, Farrer MJ, Wszolek ZK, Stoessl AJ (2008). Progression of dopaminergic dysfunction in a LRRK2 kindred: a multitracer PET study. Neurology 71: 1790-1795.
Troiano AR, de la Fuente-Fernandez R, Sossi V, Schulzer M, Mak E, Ruth TJ, Stoessl AJ (2009). PET demonstrates reduced dopamine transporter expression in PD with dyskinesias. Neurology 72: 1211-1216.†
Nandhagopal R, Kuramoto L, Schulzer M, Mak E, Cragg J, Lee CS, McKenzie J, McCormick S, Samii A, Troiano A, Ruth TJ, Sossi V, de la Fuente-Fernandez R, Calne DB, Stoessl AJ (2009). Longitudinal progression of sporadic Parkinson's disease: a multi-tracer positron emission tomography study. Brain 132: 2970-2979.
Lidstone SC, Schulzer M, Dinelle K, Mak E, Sossi V, Ruth TJ, de la Fuente-Fernandez R, Phillips AG, Stoessl AJ (2010). Great expectations: placebos mimic the effect of active medication in Parkinsonís disease. Arch Gen Psychiatry 67: 857-865.
Sossi V, de la Fuente-Fernandez R, Nandhagopal R, Schulzer M, McKenzie J, Ruth TJ, Aasly JO, Farrer MJ, Wszolek ZK, Stoessl AJ (2010). Dopamine turnover increases in asymptomatic LRRK2 mutation carriers. Movement Disorders 15: 2717-2723.
de la Fuente-Fernandez R, Schulzer M, Kuramoto L, Cragg J, Nandhagopal R, Au WL, Mak E, McKenzie J, McCormick S, Sossi V, Ruth TJ, Lee CS, Calne DB, Stoessl AJ (2011). Age specific patterns of progression of nigrostriatal dysfunction in Parkinsonís disease. Ann Neurol. 69: 803-810.
Nandhagopal R, Kuramoto L, Schulzer M, Mak E, Cragg J, McKenzie J, McCormick S, Ruth T, Sossi V, de la Fuente-Fernandez R, Stoessl AJ (2011). Longitudinal evolution of compensatory changes in striatal dopamine processing in Parkinsonís disease. Brain 134: 3290-3298.
Stoessl AJ, Lehericy S, Strafella AP. Imaging insights into basal ganglia function, Parkinson's disease, and dystonia. Lancet. 2014 384(9942):532-44.
Stoessl AJ (2015). Central pharmacokinetics of levodopa: lessons from imaging studies. Mov Disord 30: 73-79.