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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).

Molecular Biology and Biochemistry Group

The research focus currently resides on unravelling the function and disease related dysregulation of the mitochondrial Parkinson’s Disease (PD) related protein kinase PINK1. Mutations in PINK1 are associated with early onset PD (EOPD) and are the second most common cause of recessive disease. In the past few years our understanding of PINK1 function has grown significantly and PINK1 has been linked to numerous cellular functions such as neuroprotection, mitochondrial fission-fusion and mitochondrial clearance through mitophagy, to name a few. Recently, though cellular and proteomic approaches Dr Deas has identified a number of novel PINK1 protein interactors and the current focus of her work is to explore the significance of these interactions with respect to disease.

A series of molecular biology and biochemical techniques are employed within the laboratory including: western blot, SDS-PAGE, Phos-tag gel analysis of phosphorylated proteins, patient DNA sequencing, cloning, protein interaction studies and kinase assays.

At present a variety of cell and animal models are utilised including human fetal ventral mesencephalon stem cells (ReNCells - which can be differentiated into dopaminergic neurons), primary patient fibroblasts and primary mouse neuronal cultures.

Molecular Biology and Biochemistry Group figure 1 Molecular Biology and Biochemistry Group figure 2 Molecular Biology and Biochemistry Group figure 3

Page last modified on 21 jan 11 10:08