Natalie Connor-Robson
Career Development Fellow
Research Interests
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 and eventually new treatments. I am particularly interested in the role of the endocytic pathway.
My work uses genetic models of PD and I focus mainly on the roles of Glucocerebrosidase (GBA) and LRRK2 in the development of PD.
Biography
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.
Recent publications
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GABA uptake transporters support dopamine release in dorsal striatum with maladaptive downregulation in a parkinsonism model.
Journal article
Roberts BM. et al, (2020), Nat Commun, 11
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CLR01 protects dopaminergic neurons in vitro and in mouse models of Parkinson's disease.
Journal article
Bengoa-Vergniory N. et al, (2020), Nat Commun, 11
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β-synuclein promotes synaptic vesicle dopamine uptake and rescues dopaminergic neurons from MPTP-induced death
Journal article
Ninkina N. et al, (2020)
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L-type calcium channel contribution to striatal dopamine release is governed by calbindin-D28K, the dopamine transporter, D2-receptors, α2δ-subunits and sex differences
Journal article
Brimblecombe KR. et al, (2020)
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Recommendations for measuring whisker movements and locomotion in mice with sensory, motor and cognitive deficits.
Journal article
Simanaviciute U. et al, (2020), J Neurosci Methods, 331
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"LRRK2: Autophagy and Lysosomal Activity".
Journal article
Madureira M. et al, (2020), Front Neurosci, 14
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Astrocytic striatal GABA transporter activity governs dopamine release and shows maladaptive downregulation in early parkinsonism
Journal article
Roberts BM. et al, (2019)
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An integrated transcriptomics and proteomics analysis reveals functional endocytic dysregulation caused by mutations in LRRK2.
Journal article
Connor-Robson N. et al, (2019), Neurobiol Dis, 127, 512 - 526
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RNA sequencing reveals MMP2 and TGFB1 downregulation in LRRK2 G2019S Parkinson's iPSC-derived astrocytes.
Journal article
Booth HDE. et al, (2019), Neurobiol Dis, 129, 56 - 66
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LRRK2 interacts with the vacuolar-type H+-ATPase pump a1 subunit to regulate lysosomal function.
Journal article
Wallings R. et al, (2019), Hum Mol Genet