Jay has had the opportunity to investigate different aspects of brain dysfunction in a variety of labs around the world. He first gained experience with neurodevelopment and neurodegeneration research during his BSc and MSc at the University of Alberta in Edmonton, Canada. Specifically, his research on prion diseases sparked his interest in neurodegeneration and the mechanisms behind brain deterioration. This led to the pursuit of a PhD in Tübingen, Germany in the lab of Professor Mathias Jucker starting in mid-2014 (Hertie Institute for Clinical Brain Research-HIH and the German Center for Neurodegenerative Diseases-DZNE). Here, Jay focused on the biochemical features of pathological protein deposits called senile plaques that are associated with Alzheimer’s disease and are made up of β-amyloid protein. This lead to the discovery that different subtypes of Alzheimer’s disease have distinct plaque features and that the earliest forms of deposited β-amyloid protein are uniquely influential in initiating a disease cascade.
From the results of his PhD, Jay was intrigued at the heterogeneity in disease onset and the diversity of symptoms in patients suffering from neurodegenerative diseases like Alzheimer’s disease. The concept of genomic/cellular mosaicism jumped out as a currently unclear influence on how neurodegenerative diseases develop differently in the brains of an increasingly large population of patients. Jay joined the lab of Professor Geoffrey Faulkner in early 2018 to pursue this link between mosaicism and neurodegeneration in age-related diseases like Alzheimer’s disease.