Dr. Naomi Visanji is an Assistant Professor at the University of Toronto Department of Laboratory Medicine and Pathobiology and an Affiliate Scientist at the Krembil Research Institute Division of Experimental & Translational Neuroscience. Her research focuses on the use of postmortem human tissues and animal models to probe the pathobiology of neurodegenerative disease-associated proteins.
She received her BSc Hons (1st class) in Neuroscience from the University of Nottingham (UK) and completed her PhD in Pharmacology at Kings College London (UK). She has published over 50 peer-reviewed publications and has an H Index of 29. She is also a Senior Scientist at Rosetta Therapeutics, a University of Toronto/MaRS Innovation UTEST startup developing new molecular matter as leads for the cure of neurodegenerative diseases.
Dr. Visanji leads the in vivo research arm of the Rossy Program for Progressive Supranuclear Palsy at the Krembil Research Institute and the Tanz Centre for Research in Neurodegenerative Diseases.
Her research goals are to generate a sophisticated animal model that recapitulates the full spectrum of pathology exhibited in PSP to study anatomic and cytopathologic diversity in PSP, identify factors that contribute to the etiology of PSP and provide a platform for future testing of novel therapeutics.
Progressive Supranuclear Palsy (PSP) is a devastating and fatal neurodegenerative disease characterised by the abnormal accumulation of the protein tau in different cell types in select vulnerable regions of the brain.
Currently there is no animal model of PSP that replicates these hallmark pathological features of the disease, limiting our understanding of disease pathogenesis and preventing the testing of novel therapies for this disease that currently has no effective treatment.
My research program’s goals are to generate a sophisticated animal model of PSP. We will use human post mortem brain material donated by patients in the Rossy Program for Progressive Supranuclear Palsy at Toronto Western Hospital. We will extract tau protein from these human brain samples and inoculate mice that have been genetically modified to express human tau protein in a similar manner to that seen in the human brain. Using this technique we hope to generate an animal model that replicates the full spectrum of pathology exhibited in PSP.
Once established, this innovative model will provide a springboard for an array of future work, including:
- studying the role of different cell types in the spreading of tauopathy in PSP;
- identifying factors implicated in the cause of PSP; and critically,
- testing of novel disease modifying therapeutics.
α-Synuclein Strains Exhibit Key Hallmarks of Prion Strains and Initiate Distinct Transmissible Synucleinopathies in Mice. Lau, A., So, RWL., Sang, JC., Lau, HHC., Ruiz- Riquelme, RL., Stuart,E., Visanji,NP., Meisl,G., Marano, MM., Wang,Z., Fraser,PE., Tandon,A., Hyman,BT., Ingelsson,M., Klenerman,D., Watts, JC. Nat Neurosci. 2020 Jan;23(1):21-31
Beyond the synucleinopathies: Alpha synuclein as a driving force in neurodegenerative comorbidities. Visanji, NP, Lang, AE., Kovacs, GG. Translational Neurodegeneration. Sep 4;8:28.
Lacoste, AM., Bowser, R. Visanji, N.P. Disrupting drug discovery How artificial intelligence is transforming drug research. Expert Insights IBM Institute for Business Value. 2018.
Synchrotron XRF imaging of Alzheimer's disease basal ganglia reveals linear dependence of high-field magnetic resonance microscopy on tissue iron concentration. Finnegan ME, Visanji NP, Romero-Canelon I, House E, Rajan S, Mosselmans JFW, Hazrati LN, Dobson J, Collingwood JF. J Neurosci Methods. 2019 May 1;319:28-39.
Feasibility and Safety of Multicenter Tissue and Biofluid Sampling for α-Synuclein in Parkinson's Disease: The Systemic Synuclein Sampling Study (S4). Chahine LM, Beach TG, Seedorff N, Caspell-Garcia C, Coffey CS, Brumm M, Adler CH, Serrano GE, Linder C, Mosovsky S, Foroud T, Riss H, Ecklund D, Seibyl J, Jennings D, Arnedo V, Riley L, Dave KD, Mollenhauer B; Systemic Synuclein Sampling study. J Parkinsons Dis. 2018;8(4):517-527
Immunohistochemical Method and Histopathology Judging for the Systemic Synuclein Sampling Study (S4). Beach TG, Serrano GE, Kremer T, Canamero M, Dziadek S, Sade H, Derkinderen P, Corbillé AG, Letournel F, Munoz DG, White CL 3rd, Schneider J, Crary JF, Sue LI, Adler CH, Glass MJ, Intorcia AJ, Walker JE, Foroud T, Coffey CS, Ecklund D, Riss H, Goßmann J, König F, Kopil CM, Arnedo V, Riley L, Linder C, Dave KD, Jennings D, Seibyl J, Mollenhauer B, Chahine L; Systemic Synuclein Sampling Study (S4) . J Neuropathol Exp Neurol. 2018 Sep 1;77(9):793-802.
Repurposing drugs to treat L-DOPA-induced dyskinesia in Parkinson's disease. Johnston TH, Lacoste AMB, Visanji NP, Lang AE, Fox SH, Brotchie JM. Neuropharmacology. 2018 Jun 1. pii: S0028-3908(18)30270-3.
Lymphatic vasculature in human dural superior sagittal sinus: Implications for neurodegenerative proteinopathies. Visanji NP, Lang AE, Munoz DG. Neurosci Lett. 2018 Feb 5;665:18-21.
The Systemic Synuclein Sampling Study: toward a biomarker for Parkinson's disease. Visanji NP, Mollenhauer B, Beach TG, Adler CH, Coffey CS, Kopil CM, Dave KD, Foroud T, Chahine L, Jennings D; Systemic Synuclein Sampling Study (S4). Biomark Med. 2017 Apr;11(4):359-368.
AAV1/2-induced overexpression of A53T-α-synuclein in the substantia nigra results in degeneration of the nigrostriatal system with Lewy-like pathology and motor impairment: a new mouse model for Parkinson's disease. Ip CW, Klaus LC, Karikari AA, Visanji NP, Brotchie JM, Lang AE, Volkmann J, Koprich JB. Acta Neuropathol Commun. 2017 Feb 1;5(1):
α–synuclein-based animal models of Parkinson's disease: challenges and opportunities in a new era. N. P. Visanji, J. M. Brotchie, L. V. Kalia MD, J. Koprich, A. Tandon, J. C. Watts & A. E. Lang. Trends In Neuroscience Trends Neurosci. 2016 Nov;39(11):750-762
The relevance of pre-motor symptoms in Parkinson's disease. Visanji NP, Marras C. Expert Rev Neurother. 2015 Oct;15(10):1205-17. doi: 10.1586/14737175.2015.1083423. Epub 2015 Sep 1.
Deep brain stimulation of the subthalamic nucleus preferentially alters the translational profile of striatopallidal neurons in an animal model of Parkinson's disease. Visanji NP, Kamali Sarvestani I, Creed MC, Shams Shoaei Z, Nobrega JN, Hamani C, Hazrati LN. Front Cell Neurosci. 2015 Jun 9;9:221.
Gastrointestinal dysfunction in Parkinson's disease. Fasano A, Visanji NP, Liu LW, Lang AE, Pfeiffer RF. Lancet Neurol. 2015 Jun;14(6):625-39. 15. Colonic mucosal a-synuclein lacks specificity as a biomarker for Parkinson disease. Visanji NP, Marras C, Kern DS, Al Dakheel A, Gao A, Liu LW, Lang AE, Hazrati LN. Neurology. 2015 Feb 10;84(6):609-16.