Chelsie completed a combined Bachelor’s degree in Biology and Psychology at the University of Victoria. Following graduation, she worked as Interview Supervisor for the Alzheimer’s Drug Therapy Caregiver Study based at the Centre on Aging during which time she spoke with thousands of individuals across BC who provide care to family members with neurodegenerative diseases. Once the study wrapped up, she decided to pursue her passion for cellular and molecular neuroscience, with a focus on neurodegeneration, in hopes of helping find more effective treatments. She started her PhD in Neuroscience at the University of British Columbia, under the supervision of Dr. Austen Milnerwood and Dr. Matthew Farrer at the Centre for Applied Neurogenetics, where she began investigating how protein recycling pathways are altered in Parkinson’s disease and how that impacts synaptic transmission. She moved to Montreal in October 2016 to help Dr. Milnerwood start his new laboratory at McGill University, where she will continue her PhD studies at the Montreal Neurological Institute. In her spare time Chelsie enjoys running, sliding, and rolling down mountains, being punched in the face by the ocean, testing the hypothesis that she is invincible, sprinkling glitter on things, and painting pretty pictures.

VPS35 is part of the retromer complex – a protein complex involved in sorting and recycling transmembrane cargoes from maturing endosomes. Mutations in Vacuolar Protein Sorting 35 (VPS35) have been linked to late-onset, autosomal-dominant Parkinson’s disease (PD) that is clinically indistinguishable from idiopathic PD. This begs the question, what specific functions might VPS35 have in neurons that makes them more vulnerable to changes in protein recycling than other cell types? Recent work in neurons has shown that numerous neurotransmitter receptors are recycled by the retromer, including AMPA-type glutamate receptors and dopamine receptors. Chelsie’s project is to study AMPA and dopamine receptor trafficking and synaptic transmission in cultured neurons from a knock-in mouse model of the D620N mutation in VPS35, to describe how the mutation affects synapse maintenance and receptor recycling. She uses a combination of protein biochemistry, immunocytochemistry, live-cell imaging, and electrophysiology to achieve these research aims. Furthermore, she hopes to uncover the mechanism of this dysfunction, pointing to potential targets for therapeutic intervention. Studies of other PD-implicated proteins have also pointed to endosomal/vesicle trafficking mechanisms and synaptic dysfunction as a point of convergence for causal factors in PD.