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
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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...
Mutations in LRRK2 are the most common genetic cause of Parkinson’s disease. Here, Claudia Manzoni talks about her research (funded by the Rosetrees Trust and the Michael J. Fox Foundation) into what LRRK2 might be doing within the cell: Parkinson’s disease is a brain illness that afflicts 1 in 500 people in the UK. High profile patients, such as the actor Michael J Fox, the boxer Muhammad Ali and the late Pope John Paul II, have raised public awareness of Parkinson’s and its devastating impact. More...
(Alzheimer's Research Trust Research Fellow)
I studied Biochemistry and Biological Chemistry at the University of Nottingham, where I first became interested in neurodegenerative disease after undertaking a project in Dr Rob Layfield’s laboratory, examining the role of Parkin in Parkinson’s disease. After graduating in 2004, I joined Dr Diane Hanger’s lab at the MRC Centre for Neurodegeneration Research, King’s College London, where I first became interested in the role of the microtubule protein tau in neurodegenerative disease. My PhD was awarded in 2008, and in 2009 I subsequently joined Professor John Hardy’s group in the Department of Molecular Neuroscience, where I am involved in multiple projects investigating the molecular mechanisms of frontotemporal lobar degeneration. My research continues to have a particular focus on tau-mediated neurodegeneration and I was recently awarded a research fellowship from the Alzheimer’s Research Trust to support this work. In addition to my research projects, I also coordinate a BUPA/Alzheimer’s Society funded project (led by Professor Martin Rossor) which aims to generate a biobank of familial dementia patient-derived cell lines.
Page last modified on 20 mar 13 16:58