Dr. Kalia completed her combined MD/PhD training at the University of Toronto. Her doctoral research was performed under the supervision of Dr. Michael Salter at the Hospital for Sick Children. She pursued residency training in neurology at the University of Toronto and postdoctoral research at the MassGeneral Institute for Neurodegenerative Disease at Harvard University with Dr. Pamela McLean. Dr. Kalia returned to Toronto to continue her training as a movement disorders fellow at the Toronto Western Hospital with Dr. Anthony Lang.
Dr. Kalia is an assistant professor in the Division of Neurology, Department of Medicine at the University of Toronto. She is a clinician scientist at the Toronto Western Hospital, University Health Network with appointments at the Krembil Research Institute (Krembil), Tanz Centre for Research in Neurodegenerative Diseases, and Department of Laboratory Medicine and Pathobiology.
Her research program focuses on Parkinson’s disease and aims to understand the key molecular pathways responsible for neurodegeneration to develop novel therapies. Her lab uses a comprehensive approach involving molecular biology techniques, in vitro biochemical assays, cellular models, and in vivo animal models. Her clinical practice is dedicated to the care of patients with Parkinson’s disease and related disorders. Thus she is in an ideal position: 1) to utilize observations made in the clinic to generate hypotheses that can be tested in the lab; and, 2) to translate lab discoveries to have positive impacts on the lives of patients with neurodegenerative disorders.
Industry Expertise (3)
Health Care - Services
Areas of Expertise (8)
University of Toronto: Ph.D., Neuroscience 2006
Queen's University: B.S., Biology 1997
Media Appearances (1)
Dr. Suneil Kalia: The long quest for a Parkinson’s cure
Lorraine Kalia offered clinical perspectives during the question and answer portion of the presentation ...
In this review, we summarize the clinical trials of disease-modifying therapies for PD that were published since 2013 as well as clinical trials currently in progress. We also discuss promising approaches and ongoing challenges in this area of PD research.
The role of protein aggregates, such as Lewy body inclusions, in the molecular pathogenesis of Parkinson's disease has remained controversial and elusive. The protein α-synuclein is a major component of these inclusions but it can exist in many alternate conformations. Here we review advances in our understanding of the roles of Lewy pathology and α-synuclein in Parkinson's disease.
We studied suggestion of benefit combined with motor cortex and premotor cortex repetitive transcranial magnetic stimulation (rTMS) in chronic (>2 years) FMDs.
Mutations in leucine-rich repeat kinase 2 (LRRK2) are the most common cause of genetic Parkinson disease (PD) known to date. The clinical features of manifesting LRRK2 mutation carriers are generally indistinguishable from those of patients with sporadic PD. However, some PD cases associated with LRRK2 mutations lack Lewy bodies (LBs), a neuropathological hallmark of PD. We investigated whether the presence or absence of LBs correlates with different clinical features in LRRK2-related PD.
Mutations in leucine-rich repeat kinase 2 (LRRK2) cause inherited Parkinson disease (PD), and common variants around LRRK2 are a risk factor for sporadic PD. Using protein-protein interaction arrays, we identified BCL2-associated athanogene 5, Rab7L1 (RAB7, member RAS oncogene family-like 1), and Cyclin-G-associated kinase as binding partners of LRRK2.