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John Hardy, PhD, right, accepted the 2015 Robert A. Pritzker Prize from MJFF VP Brian Fiske, PhD, and Michael J. Fox on April 15.

John Hardy awarded 2015 Robert A. Pritzker Prize for Leadership in Parkinson's Research

One of the UK Parkinson's Disease Consortium Principal Investigators, Prof John Hardy, has been awarded the 2015 Robert A. Pritzker Prize for his leadership in Parkinson's genetics research. The award was presented by Michael J. Fox at a ceremony in New York on April 15. From the Michael J. Fox Foundation website: More...

Webcast - Prof Nicholas Wood - Advances in Genetic Understanding of Parkinson's Disease.

Video: Advances in Genetic Understanding of Parkinson's Disease

Webcast of the presentation entitled ‘Advances in Genetic Understanding of Parkinson's Disease’ given by Nicholas Wood (University College London, United Kingdom) presented at the Biochemical Society Hot Topic event, PINK1-Parkin Signalling in Parkinson’s Disease and Beyond, held in December 2014. More...

Pedigrees and I-FP-CIT SPECT scan images of the four families with GCH1 mutations involved in this study.

GCH1 gene and Parkinson's risk

A study published in Brain, led by researchers at UCL Institute of Neurology, has shown that genetic mutations which cause a decrease in dopamine production in the brain and lead to a form of childhood-onset Dystonia, also play a role in the development of Parkinson’s disease.
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Leonard Wolfson Experimental Neurology Centre (LWENC)

The new Leonard Wolfson Experimental Neurology Centre (LWENC) has opened for clinical studies and trials

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Audioslide presentation on Claudia Manzoni's paper examining how fibroblasts with LRRK2 mutations react to starvation conditions and the possible deficits that they have in autophagy.

LRRK2 and autophagy in fibroblasts

In this paper Claudia Manzoni studies how fibroblast cells from people with Parkinson’s disease caused by mutations in LRRK2 react to starvation. Although the changes are quite subtle, there are differences between the way that fibroblasts that contain mutant LRRK2 respond to being starved – suggesting that there may be changes in the way that these cells regulate a key process called autophagy (a term which comes from the greek meaning to eat yourself, and is one of the ways that cells get rid of waste and recycle proteins and organellles).
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Protein Phosphorylation Group

Protein kinases are the largest family of enzymes encoded by the human genome and their role is to catalyse the covalent attachment of phosphate to specific amino acid residues in target proteins. This modifies the functions of the target proteins in almost all conceivable way and hence the physiological processes in which they participate.

Recent clinical studies have identified alterations in genes that encode many kinases which cause striking diseases including cancer, hypertension and Parkinson’s disease (Fig 1). Little is known about how many of these kinases are regulated and how they operate in normal cells. The aim of our research is aimed at understanding the regulation and function of some of these enzymes and how their mutation leads to disease. We hope this information will lead to new fundamental understanding of the causes of disease that might be exploited to develop new approaches to better treat or even cure these diseases. Our laboratory utilizes the state of the art biochemistry, mouse genetics-physiology, mass spectrometry and signal transduction technology to address these questions

List of human diseases caused by mutations in protein kinases

Figure 1 Human Diseases Caused by Mutations in Protein Kinases


Lab website

Page last modified on 27 jan 11 16:34