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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).

Direct Observation of the Interconversion of Normal and Toxic Forms of a-Synuclein

27 June 2012

UCL Institute of Neurology Parkinson’s Disease (PD) experts Dr Emma Deas, Dr Andrey Abramov and Professor Nicholas Wood joined forces with prominent Cambridge biophysicists Dr Nunilo Cremades, Professor David Klenerman FRS and Professor Christopher Dobson FRS to identify the pathological species of alpha-synuclein responsible for nerve cell damage during disease.

Together, they identified that the structural conversion of alpha-synuclein aggregates from alpha-helical to high beta-sheet content was highly damaging to nerve cells.  These exciting results were published last month in the prestigious scientific journal “Cell”.

This important discovery not only advances our current understanding of the disease but also lays the foundation for the development of novel drug therapies, which can specifically ‘attack’ this species of alpha-synuclein to prevent nerve cell damage occurring.

Cell work: Type B oligomers induce high aberrant levels of ROS


Direct Observation of the Interconversion of Normal and Toxic Forms of α-Synuclein

Nunilo Cremades, Samuel I.A. Cohen, Emma Deas, Andrey Y. Abramov, Allen Y. Chen, Angel Orte, Massimo Sandal, Richard W. Clarke, Paul Dunne, Francesco A. Aprile, Carlos W. Bertoncini, Nicholas W. Wood, Tuomas P.J. Knowles, Christopher M. Dobson, David Klenerman

Cell - 25 May 2012 (Vol. 149, Issue 5, pp. 1048-1059)

Page last modified on 27 jun 12 10:59