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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).

Adamantios Mamais

(Research Associate)

Adamantios Mamais

I hold a multi-disciplinary research background having had the opportunity to study and investigate many aspects of cell biology leading to human disease. Having completed a BSc in Molecular Biology at University College London in 2001, I pursued an MSc in Molecular Medicine, at the same university, that equipped me with a deeper understanding of the underlying mechanisms and consequences that give rise to pathology, when the blue-prints of nature go wrong.

My academic studies cultivated my enthusiasm on the molecular events of human disease, while I had the chance to work on proteins involved in gastrulation and synaptic neurotransmission, and also tumour targeting drugs, during my BSc/MSc research projects respectively. During a summer placement at the UCL Institute of Neurology I was involved in a project investigating the mechanistics of filopodia formation in developing neurons. I then joined the Institute of Cancer Research for two years as a Scientific Officer to investigate nucleosomal positioning and chromatin remodelling mechanisms in V(D)J recombination. In 2005 I focused my research skills and experience in pursuing a PhD at the UCL Institute of Neurology, in the lab of Prof Louis Lim and Dr Christine Hall, investigating novel mechanisms of interplay between cytoskeletal remodelling factors involved in neuronal differentiation and mRNA binding factors involved in local translation in axons and formation of Stress Granules.

In 2010, I joined the team of Dr Rina Bandopadhyay and Dr Patrick Lewis at the Reta Lila Weston Institute, UCL Institute of Neurology, as a post-doc Research Associate, and I am currently investigating the molecular events that underlie LRRK2 associated Parkinson’s disease. My research utilises the invaluable resource of post-mortem human brain tissue from Parkinson’s cases, provided by the Queen Square Brain Bank. We are focusing on the post-translational modifications and neuropathological features of two LRRK2 putative partners in disease, a-Synuclein and 4E-BP1. Furthermore, I have initiated a novel project investigating the role of mutated LRRK2 in mRNA Stress Granule formation, recently involved in pathologic protein aggregation in neurodegenerative diseases.

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