UK Parkinson's Disease Consortium - UKPDC
- Principal Investigators
- Research Groups
- Cell Physiology
- Clinical Neuroscience
- Clinical Studies
- Drosophila Genetics
- Molecular Biology and Biochemistry
- Molecular Neuropathology
- Neurological Biochemistry
- Neurological Signalling
- Protein Phosphorylation
- Contact us
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...
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.
The new Leonard Wolfson Experimental Neurology Centre (LWENC) has opened for clinical studies and trials
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).
Research led by consortium researchers Dr Helene Plun-Favreau (UCL Institute of Neurology) and Dr Alex Whitworth (University of Sheffield), and collaborator Dr Heike Laman (University of Cambridge), has discovered how genetic mutations linked to Parkinson’s disease might play a key role in the death of brain cells, potentially paving the way for the development of more effective drug treatments. In the new study, published in Nature Neuroscience, the team of cross-institutional researchers showed how defects in the Parkinson’s gene Fbxo7 cause problems with mitophagy. More...
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.
|Link to publications|