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.
An integrated transcriptomics and proteomics analysis reveals functional endocytic dysregulation caused by mutations in LRRK2.
Connor-Robson N. et al, (2019), Neurobiol Dis, 127, 512 - 526
RNA sequencing reveals MMP2 and TGFB1 downregulation in LRRK2 G2019S Parkinson's iPSC-derived astrocytes.
Booth HDE. et al, (2019), Neurobiol Dis, 129, 56 - 66
LRRK2 interacts with the vacuolar-type H+-ATPase pump a1 subunit to regulate lysosomal function.
Wallings R. et al, (2019), Hum Mol Genet
Are rodent models of Parkinson's disease behaving as they should?
Vingill S. et al, (2018), Behav Brain Res, 352, 133 - 141
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