Dr. Kalia is a graduate of the MD/PhD program at the University of Toronto, where he entered the neurosurgery residency program in 2006. During his PhD he discovered novel molecular targets which contribute to the degeneration of dopaminergic neurons in Parkinson's disease. From 2009-10, he completed a postdoctoral research fellowship at the Massachusetts General Hospital Institute for Neurodegenerative Disease, Harvard University. He subsequently resumed residency training and graduated from the Toronto program in 2012 and became a Fellow of the Royal College of Physicians and Surgeons of Canada that year.
From 2012-13, Dr. Kalia completed a clinical fellowship in functional and stereotactic neurosurgery at Toronto Western Hospital, and was recruited to the Division of Neurosurgery with a staff appointment at Toronto Western Hospital. He is appointed as an Assistant Professor in the Department of Surgery at the University of Toronto. His clinical focus on the surgical management of movement disorders, particularly Parkinson’s disease, follows as a logical extension of his longstanding research interests. His research laboratory is within the Krembil Research Institute and focuses on understanding molecular mechanisms of protein homeostasis in neurodegeneration and on establishing model systems to study protein function in neurodegenerative disease.
Dr. Kalia is married to Lorraine Kalia, a neurodegenerative disease researcher and a movement disorders neurologist at Toronto Western Hospital.
Industry Expertise (3)
Areas of Expertise (10)
CIHR Brain Star Award (professional)
Awarded by the Canadian Institutes of Health Research.
Golden Stethoscope Award (professional)
Awarded for for exceptional and compassionate clinical care by the University of Toronto.
University of Toronto: Ph.D., Neurobiology and Neurosciences 2006
McGill University: B.S., Immunology 1997
Media Appearances (2)
Dr. Suneil Kalia: The long quest for a Parkinson’s cure
It was an article about the late Wilder Penfield, a neurosurgery pioneer, that sparked a young Suneil Kalia’s quest to become a neurosurgeon three decades ago ...
Eliminating ‘bad chaperone’ proteins to find a cure for Parkinson's
Parkinson Canada online
One of the most difficult aspects of Dr. Suneil Kalia's practice as a neurosurgeon is the moment he has to tell patients treated for years at Toronto Western’s Movement Disorders Clinic that neurologists no longer have anything to offer them that will significantly relieve their symptoms of Parkinson's disease ...
The forniceal area is currently being evaluated as a target for deep brain stimulation (DBS) to improve cognitive function in patients with Alzheimer's disease. The molecular changes at downstream targets within the stimulated circuit are unknown.
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.
Dexmedetomidine (an alpha-2 adrenergic agonist) sedation is commonly used during subthalamic nucleus (STN) deep-brain stimulation (DBS). Its effects on the electrophysiological characteristics of human STN neurons are largely unknown. We hypothesised that dexmedetomidine modulates the firing rates and bursting of human STN neurons.
We report on the clinical efficacy of bilateral globus pallidus internus deep brain stimulation in two patients with myoclonus dystonia/essential myoclonus who lack mutations in the epsilon sarcoglycan gene. The primary outcome measures were the Burke-Fahn-Marsden Dystonia Scale motor severity and the Unified Myoclonus Rating Scale scores, and the secondary outcome measure was the 36-item Short Form Health Survey score at the last postoperative follow up.