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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.

Leonard Wolfson Experimental Neurology Centre (LWENC)

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


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).

Video: Parkinson's UK site visit for the Targeting LRRK2 project

1 November 2011

LRRK2 from Tony Cox on Vimeo.

LRRK2 – pronounced lark 2 – is the most common gene associated with Parkinson’s. A mutant form of LRRK2 can cause the death of nerve cells, and blocking this form of LRRK2 from working can prevent this from happening. Before we can use this knowledge to develop treatments we need to fill in the gaps in our understanding of the role LRRK2 plays when it’s healthy, and of the different proteins it interacts with along the way within the nerve cell.

Figuring out how LRRK2 works and how to change this is a promising route to developing novel therapies for the treatment and ultimately cure for Parkinson’s. Although a long way off, we hope that these can ultimately be tested in the clinic to see if we can slow down or alter the progress of the condition.

Patrick Lewis - Lead researcher for the Targeting LRRK2 project

Patrick Lewis' profile

More information (PDF) on the Targeting LRRK2 project

Page last modified on 01 nov 11 14:21