Dr. Neil Vasdev

Alzheimer disease (AD), with amyloid-β neuritic plaques and tau neurofibrillary tangles as hallmark pathologic changes, has diverse clinical manifestations, from typical amnesic disease to atypical variants including a behavioral and dysexecutive variant, posterior cortical atrophy (PCA), logopenic variant primary progressive aphasia (lvPPA), and corticobasal syndrome (CBS).¹ Although fibrillar amyloid plaques are necessary for a pathologic diagnosis of AD,² their density and distribution postmortem are weakly associated with clinical features and are not associated with markers of neurodegeneration.³^,4 This finding has been further confirmed in vivo using amyloid positron emission tomographic (PET) imaging.⁵ In contrast, postmortem neurofibrillary tangles are closely linked to clinical phenotype and regional neurodegeneration in both typical³^,4 and atypical AD.⁶^-8 With the recent development of PET ligands specifically labeling the hyperphosphorylated paired helical filament tau pathologic condition present in AD,⁹ we can now test the hypotheses regarding associations of tau localization and density with clinical features of AD in vivo.

9 July 2014 in Nature Communications

Journal Article

Spirocyclic hypervalent iodine(III)-mediated radiofluorination of non-activated and hindered aromatics

Benjamin Rotstein

Nickeisha A. Stephenson

Neil Vasdev

Steven H. Liang

1 November 2016 in JAMA Neurology

Journal Article

Tau Positron Emission Tomographic Imaging in the Lewy Body Diseases

Stephen N. Gomperts

Joseph J. Locascio

Sara J. Makaretz

Aaron Schultz

Christina Caso

Keith Johnson

Dementia with Lewy bodies (DLB), Parkinson disease (PD), and PD dementia (PDD) together compose the Lewy body diseases, which are defined neuropathologically by Lewy body intracellular inclusions that are rich in α-synuclein.¹ In individuals with DLB and PDD, coexistent Alzheimer disease (AD) pathologic changes, in the form of extracellular amyloid plaques and intracellular paired helical filaments of tau, are commonly observed at autopsy.²^-6 The relevance of these protein aggregates to the course of the diseases has been based primarily on clinicopathologic correlations. With the advent of positron emission tomographic (PET) molecular imaging, it is possible to examine both the timing and extent to which amyloid and tau affect cognition during life in the course of disease.⁷^,8

About Me

Dr. Neil Vasdev is the Director and Chief Radiochemist of the Brain Health Imaging Centre at CAMH. He is also the inaugural Director of the Azrieli Centre for Neuro-Radiochemistry. He is the endowed Azrieli Chair in Brain and Behaviour, and Tier 1 Canada Research Chair in Radiochemistry and Nuclear Medicine. In addition, he is a full Professor in the Department of Psychiatry at the University of Toronto. Prof. Vasdev started his radiochemistry and neuroimaging training while obtaining his Bachelor degrees (summa cum laude) in Chemistry and Psychology at McMaster University. He completed his Ph.D. dissertation in Chemistry while supported by the Natural Sciences and Engineering Research Council of Canada (NSERC). He continued training with a NSERC postdoctoral fellowship in the Department of Nuclear Medicine and Functional Imaging at the E.O. Lawrence Berkeley National Laboratory in California. He began his independent faculty career in radiopharmaceutical sciences at CAMH/University of Toronto in 2004. From 2011 to 2017, he served as the Director of Radiochemistry and at the Massachusetts General Hospital and an Associate Professor in the Department of Radiology at Harvard Medical School. Dr. Vasdev was elected as a Fellow of the American Chemical Society (2020), Royal Society of Chemistry (2020), and Society of Nuclear Medicine and Molecular Imaging (2021) for his outstanding achievements and contributions to science, the profession and the societies.

Dr. Neil Vasdev

Dr. Neil Vasdev

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About Me