Postdoctoral Career Development Fellow
As part of the Oxford Parkinson’s disease centre my research is based around characterising the earliest pathogenic changes that occur in Parkinson’s disease (PD) and trying to understand how this leads to disease. I am investigating how these molecular alterations lead to and cause the progression of the disease with the hope that this will allow us to develop a much better understanding of Parkinson’s.
My work uses genetic models of PD and I am particularly interested in Glucocerebrosidase (GBA). It is well known that people who are heterozygous for mutations in GBA have a higher risk of developing PD but why these mutations lead to the disease is currently poorly understood.
I studied Biomedical Sciences at Cardiff University graduating in 2009 and going on to complete my PhD in 2013 at the same university. My PhD also concentrated on the mechanisms of Parkinson’s disease with particular interest in a loss of function role for alpha-synuclein.
Are rodent models of Parkinson's disease behaving as they should?
Vingill S. et al, (2017), Behav Brain Res
Combinational losses of synucleins reveal their differential requirements for compensating age-dependent alterations in motor behavior and dopamine metabolism.
Connor-Robson N. et al, (2016), Neurobiol Aging, 46, 107 - 112
Forced cell cycle exit and modulation of GABAA, CREB, and GSK3β signaling promote functional maturation of induced pluripotent stem cell-derived neurons.
Telezhkin V. et al, (2016), Am J Physiol Cell Physiol, 310, C520 - C541
LRRK2 BAC transgenic rats develop progressive, L-DOPA-responsive motor impairment, and deficits in dopamine circuit function.
Sloan M. et al, (2016), Hum Mol Genet, 25, 951 - 963
A novel resource for studying function and dysfunction of α-synuclein: mouse lines for modulation of endogenous Snca gene expression.
Ninkina N. et al, (2015), Sci Rep, 5