Professor Joanne E. Nash

Joanne E. Nash

Associate Professor



CSB Appointment


Research Areas



Ph.D. University of Manchester (UK) 1999
M.Sc.. University of Manchester (UK) 1996
B.Sc. (Hons) University of Aberdeen (UK) 1995

Primary Undergraduate Department

Biological Sciences, UTSC

Graduate Programs

Cell & Systems Biology
Ecology & Evolutionary Biology

Academic or Administrative Appointments

Program Supervisor for Cell and Molecular Biology (UTSC campus)

Research Description

We employ a multidisciplinary approach to understand the cell and molecular mechanisms underlying neurological diseases such as Parkinson’s disease. It is hoped that these studies will lead to better treatments for patients suffering from these diseases.

Contact Information

Office Phone: 416-287-7445
Office: S532
Lab: S529
Lab Phone: 416-208-4833

Mailing Address

Department of Cell & Systems Biology
University of Toronto
1265 Military Trail
Scarborough, ON M1C 1A4



A novel MDMA analogue, UWA-101, that lacks psychoactivity and cytotoxicity, enhances L-DOPA benefit in parkinsonian primates

Johnston TH, Millar Z, Huot P, Wagg K, Thiele S, Salomonczyk D, Yong-Kee CJ, Gandy MN, McIldowie M, Lewis KD, Gomez-Ramirez J, Lee J, Fox SH, Martin-Iverson M, Nash JE, Piggott MJ, Brotchie JM
2012, FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 26, 2154-63, 22345403

Development of a unilaterally-lesioned 6-OHDA mouse model of Parkinson’s disease

Thiele SL, Warre R, Nash JE
2012, Journal of visualized experiments : JoVE, 22370630

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Generation of a model of L-DOPA-induced dyskinesia in two different mouse strains

Thiele SL, Warre R, Khademullah CS, Fahana N, Lo C, Lam D, Talwar S, Johnston TH, Brotchie JM, Nash JE
2011, Journal of neuroscience methods, 197, 193-208, 21352853

LTP in hippocampal neurons is associated with a CaMKII-mediated increase in GluA1 surface expression

Appleby VJ, Corrêa SA, Duckworth JK, Nash JE, Noël J, Fitzjohn SM, Collingridge GL, Molnár E
2011, Journal of neurochemistry, 116, 530-43, 21143596

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Altered function of glutamatergic cortico-striatal synapses causes output pathway abnormalities in a chronic model of parkinsonism

Warre R, Thiele S, Talwar S, Kamal M, Johnston TH, Wang S, Lam D, Lo C, Khademullah CS, Perera G, Reyes G, Sun XS, Brotchie JM, Nash JE
2011, Neurobiology of disease, 41, 591-604, 20971190

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Disruption of the interaction between myosin VI and SAP97 is associated with a reduction in the number of AMPARs at hippocampal synapses

Nash JE, Appleby VJ, Corrêa SA, Wu H, Fitzjohn SM, Garner CC, Collingridge GL, Molnár E
2010, Journal of neurochemistry, 112, 677-90, 19895665

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To serve and protect? Interventions in the subthalamic nucleus for Parkinson’s disease. Commentary on “Ablation of the subthalamic nucleus protects dopaminergic phenotype but not cell survival in a rat model of Parkinson’s disease”

Kalia SK, Nash JE, Lozano AM
2004, Experimental neurology, 185, 201-3, 14736500

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Interaction of SAP97 with minus-end-directed actin motor myosin VI. Implications for AMPA receptor trafficking

Wu H, Nash JE, Zamorano P, Garner CC
2002, The Journal of biological chemistry, 277, 30928-34, 12050163

Characterisation of striatal NMDA receptors involved in the generation of parkinsonian symptoms: intrastriatal microinjection studies in the 6-OHDA-lesioned rat

Nash JE, Brotchie JM
2002, Movement disorders : official journal of the Movement Disorder Society, 17, 455-66, 12112191

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