My research focusses on alpha-synuclein aggregation and neuroinflammation in Parkinson’s disease. Even though it is known that alpha-synuclein aggregation and neuroinflammation are key features of Parkinson’s disease progression there are still many unanswered questions. Where does the toxic aggregation begin? How does it spread? Which cells respond to it? How can we prevent these processes? In order to study glial activation and the aggregation process, and answer these questions we benefit from access to genetic models, patient-derived induced pluripotent stem (iPS) cells, human tissue and alpha-synuclein PLA-based assays. This technology will help us provide novel insights of the role alpha-synuclein oligomers and glial activation play in Parkinson's and so, could be used to identify new treatments.
In 2018 I became an Oxford-BMS/Celgene Research Fellow studying alpha-synuclein aggregation and glial activation in Parkinson's. I joined the Wade-Martins laboratory in 2015 and have since worked on the role of alpha-synuclein aggregation in Parkinson’s disease. After graduating I started and Masters in Molecular Biology and Biomedicine, in which I studied the differentiation of human embryonic carcinoma stem cells. This led me to develop an interest in the use of stem cells as models for human neuronal differentiation. In 2014 I completed a PhD at the University of the Basque Country which focused on the study of the role of Wnt signaling during early neuronal differentiation in human stem cell models.
Undergraduate lecturer on Protein folding in neurodegenerative diseases for 3rd year Medical students (FHS) in the Theme “Neurology: from bench to bedside” at Oxford University.
Tutor for Stem cells and Neurodegeneration at Oxford University.
Current team: Ms Quyen Do (PhD student), Ms Naroa Ibarra-Aizpurua (PhD student) and Ms Feodora Bertherat (MSc student).
Past members: Ms Maria Knudsen (MSc student), Ms Ecem Kirkiz (undergraduate student), Ms Josse Poppinga (MSc student) and Mr Jose Maria Salazar Campos (undergraduate student).
Tau-proximity ligation assay reveals extensive previously undetected pathology prior to neurofibrillary tangles in preclinical Alzheimer's disease.
Bengoa-Vergniory N. et al, (2021), Acta Neuropathol Commun, 9
GABA uptake transporters support dopamine release in dorsal striatum with maladaptive downregulation in a parkinsonism model.
Roberts BM. et al, (2020), Nat Commun, 11
CLR01 protects dopaminergic neurons in vitro and in mouse models of Parkinson's disease.
Bengoa-Vergniory N. et al, (2020), Nat Commun, 11
Transgenic Mice Expressing Human α-Synuclein in Noradrenergic Neurons Develop Locus Ceruleus Pathology and Nonmotor Features of Parkinson's Disease.
Butkovich LM. et al, (2020), J Neurosci, 40, 7559 - 7576
Understanding the pathophysiological role of early tau aggregates in Alzheimer's disease by their direct visualisation in situ
Velentza-Almpani E. et al, (2020), NEUROPATHOLOGY AND APPLIED NEUROBIOLOGY, 46, 42 - 42