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...
Protein Phosphorylation Group
Protein kinases are the largest family of enzymes encoded by the human genome and their role is to catalyse the covalent attachment of phosphate to specific amino acid residues in target proteins. This modifies the functions of the target proteins in almost all conceivable way and hence the physiological processes in which they participate.
Recent clinical studies have identified alterations in genes that encode many kinases which cause striking diseases including cancer, hypertension and Parkinson’s disease (Fig 1). Little is known about how many of these kinases are regulated and how they operate in normal cells. The aim of our research is aimed at understanding the regulation and function of some of these enzymes and how their mutation leads to disease. We hope this information will lead to new fundamental understanding of the causes of disease that might be exploited to develop new approaches to better treat or even cure these diseases. Our laboratory utilizes the state of the art biochemistry, mouse genetics-physiology, mass spectrometry and signal transduction technology to address these questions
Figure 1 Human Diseases Caused by Mutations in Protein Kinases
Page last modified on 27 jan 11 16:34