Suneil Kalia, PhD, MD

Suneil Kalia, MD, PhD, FRCS(C), is a scientist at Krembil Research Institute and Assistant Professor in Neurosurgery at the University of Toronto. His research laboratory focuses on understanding molecular mechanisms of protein homeostasis in neurodegeneration and on establishing model systems to study protein function in Parkinson’s disease (PD). As a neurosurgeon his clinical focus is on the surgical management of movement disorders, particularly PD.

Dr. Kalia received his BSc at McGill University and his MD and PhD degrees from the University of Toronto. In 2006 he entered the neurosurgery residency program at University of Toronto, during which he completed a postdoctoral research fellowship at the Massachusetts General Hospital Institute for Neurodegenerative Disease at Harvard University. After obtaining his FRCS(C) in neurosurgery, he undertook subspecialty training in stereotactic and functional neurosurgery at the Toronto Western Hospital.

His team is actively working on developing novel biological therapies that are designed to slow or halt the progression of neurodegeneration in PD.
Parkinson’s disease (PD) is a disabling movement disorder that affects between 1-3% of the Canadian population over the age of 65. Poor handling and elimination of misfolded proteins has been identified as central in the molecular pathogenesis of PD. A special class of proteins within the cell called “chaperones” is responsible for refolding misfolded or damaged proteins. If the chaperone system cannot adequately deal with these misfolded proteins, they are targeted to specialized disposal systems in the cell including the ubiquitin-proteasome system and the autophagy-lysosomal system. Together these pathways are critical to maintain protein quality control within a cell. If they are dysfunctional or overwhelmed then neurodegeneration ensues.
 
Our current work is aimed at:
1)      Understanding how chaperone molecules fail to maintain adequate protein quality control in PD and other neurodegenerative disorders;
2)      Dissecting molecular pathways that contribute to aberrant protein disposal via the proteasome and lysosomal systems in PD; and,
3)      Developing innovative methods to target and regulate these protein quality control pathways in PD and other neurodegenerative disorders.
 
Our ultimate goal is to find ways to mitigate the loss of neurons in the brain to be able to slow or even halt the progression of PD and other neurodegenerative disorders.
Dev Med Child Neurol. 2018 Oct 15;:
Elkaim LM, Alotaibi NM, Sigal A, Alotaibi HM, Lipsman N, Kalia SK, Fehlings DL, Lozano AM, Ibrahim GM, North American Pediatric DBS Collaboration
Expert Rev Neurother. 2018 Sep 15;:
Elkaim LM, De Vloo P, Kalia SK, Lozano AM, Ibrahim GM
Brain Stimul. 2018 Aug 23;:
Fomenko A, Neudorfer C, Dallapiazza RF, Kalia SK, Lozano AM
Ann Neurol. 2018 Aug 28;:
Ghahremani A, Aron AR, Udupa K, Saha U, Reddy D, Hutchison WD, Kalia SK, Hodaie M, Lozano AM, Chen R
Brain. 2018 Jun 05;:
Milosevic L, Kalia SK, Hodaie M, Lozano AM, Popovic MR, Hutchison WD
Expert Rev Neurother. 2018 May 21;:
Cury RG, Kalia SK, Shah BB, Jimenez-Shahed J, Prashanth LK, Moro E
Mov Disord. 2018 Feb 24;:
Meng Y, Voisin MR, Suppiah S, Kalia SK, Kalia LV, Hamani C, Lipsman N
Ann Neurol. 2018 Jan 25;:
Ni Z, Kim SJ, Phielipp N, Ghosh S, Udupa K, Gunraj CA, Saha U, Hodaie M, Kalia SK, Lozano AM, Lee DJ, Moro E, Fasano A, Hallett M, Lang AE, Chen R
Brain Stimul. 2017 Nov 23;:
Mann A, Gondard E, Tampellini D, Milsted JAT, Marillac D, Hamani C, Kalia SK, Lozano AM

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Assistant Professor University of Toronto