Postdoctoral Research Scientist
We focus on understanding the mechanisms behind Parkinson’s disease (PD) using induced pluripotent stem (iPS) cells lines generated through the Oxford Parkinson’s disease Centre (OPDC). My main project focus on the mechanisms behind uptake and propagation of alpha synuclein in neurons derived from healthy individuals and PD patients. We use this system to investigate pathways that are differentially influenced by alpha synuclein in patient and control neurons. The insight we gain will then allow us to develop iPS cells as a drug testing platform for novel Parkinson’s therapies.
I come from Vingelen, Norway and did a BSc in Molecular Biology at the University of Oslo. I then continued with an MSc in Neuroscience at the International Max-Planck Research School in Göttingen, Germany, where I also did my PhD. My thesis focused on the characterization of novel mouse models for Parkinsonian Pyramidal Syndrome (PARK15) in the Stegmüller lab at the Max-Planck Institute of Experimental Medicine. In July 2016 I joined the Wade-Martins lab as a postdoctoral research scientist.
Impairment of Macroautophagy in Dopamine Neurons Has Opposing Effects on Parkinsonian Pathology and Behavior.
Hunn BHM. et al, (2019), Cell Rep, 29, 920 - 931.e7
Myelinating Glia-Specific Deletion of Fbxo7 in Mice Triggers Axonal Degeneration in the Central Nervous System Together with Peripheral Neuropathy.
Joseph S. et al, (2019), J Neurosci, 39, 5606 - 5626
Are rodent models of Parkinson's disease behaving as they should?
Vingill S. et al, (2018), Behav Brain Res, 352, 133 - 141
Loss of FBXO7 (PARK15) results in reduced proteasome activity and models a parkinsonism-like phenotype in mice.
Vingill S. et al, (2016), EMBO J, 35, 2008 - 2025
Distinct subsets of Syt-IV/BDNF vesicles are sorted to axons versus dendrites and recruited to synapses by activity.
Dean C. et al, (2012), J Neurosci, 32, 5398 - 5413