I am a molecular neuroscientist with a broad training and a wide range of scientific interests. I moved to the OU in April 2015 and am currently setting-up my lab.
I began my career with a BSc in Medical Biochemistry at The University of Leicester, UK (1995-1998), followed by an MSc in International Biotechnology taught jointly by De Montfort University, UK, and the Hogeschool Brabant, the Netherlands (1998-1999). I subsequently undertook a PhD in at the University of Bristol, UK (1999-2003). I also hold a Graduate Certificate in Statistics obtained part-time from Birkbeck, University of London (2009-2010). My first post-doc was at Columbia University, USA (2003-2005), studying the molecular mechanisms of learning and memory. This was followed by posts at the UCL Institute of Child Health, UK (2006-2009), investigating gene expression and neurogenesis, and The School of Pharmacy (now UCL School of Pharmacy), UK (2009-2015), studying the role of deregulated Wnt signalling in the aetiology of Parkinson’s disease.
The long-term aim for my research is to develop and utilize state-of-the-art cellular models to study Parkinson’s disease (PD). PD is an incurable neurodegenerative disease that greatly decreases the quality of life of its sufferers and of their families. I am most interested in uncovering the earliest molecular events occurring in this condition, which happen before neurons have died and diagnosable symptoms are present. Targeting these events represents the only realistic non-surgical approach to curing the disease.
My recent work has focused on Leucine-rich repeat kinase 2 (LRRK2). Although PD risk is predominantly conferred by environmental factors, mutations in the LRRK2 gene are the most common known cause of PD. Working with Kirsten Harvey at the UCL School of Pharmacy, I have found strong evidence that LRRK2 plays a role in the canonical Wnt signaling pathway. Most importantly, PD-causing mutations in LRRK2 weaken Wnt signaling, whilst our soon-to-be-published data indicate that a protective mutation has the opposite effect, increasing the strength of this signal transduction pathway. These results are remarkable given the growing number of genes linked to both PD and the canonical Wnt pathway (e.g. LRRK2, Parkin, VPS35 and others). Furthermore, the evidence for a key role for Wnt signaling for the normal functioning and survival of cells in a healthy brain is accumulating all the time. Thus my work is at the forefront of an exciting story that implicates deregulated Wnt signaling in the pathology of PD.
I am currently setting up my lab at the OU with two major focuses: 1) research into the effect of PD-causing mutations and environmental factors on Wnt signaling; 2) the use of unbiased comparative approaches to determine common consequences of PD-causing mutations. Beyond these, I have a wide range of interests including the application of mathematics to biology, cell signaling and kinase biology, gene transcription and vesicle trafficking. I am also interested in other forms of neurological disease, for example Alzheimer’s disease, Huntington’s disease, and Schizophrenia.
I am keen to present my work to academic colleagues and lay people alike, and also to engage with Journalists and media professionals to enhance the impact of my work. For example, coverage of results I presented at the Society for Neuroscience conference in New Orleans in 2012 were covered in the online Alzheimer’s disease magazine, Alzforum.
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