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
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 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).
Molecular Neuropathology Group
Our current research focuses on understanding the normal biology and pathogenic properties of key molecules associated with familial forms of PD like LRRK2 and alpha-synuclein using our unique post-mortem human brain tissue resource at the Queen Square Brain Bank. We use a variety of approaches including cellular, immunohistochemical and biochemical techniques to understand the role of key proteins in PD pathogenesis. We hypothesize that LRRK2 can function as a protein kinase in vivo and that phosphorylation of certain key substrates is critical for mediating the downstream toxic properties of LRRK2 in neurodegeneration. Therefore one of our aims is to identify and validate in vivo phosphorylation targets of LRRK2 from our G2019S mutation cases.
In addition we are also investigating a possible role of LRRK2 in mRNA processes following up on recent publications that link this protein to mechanisms of translational control. We are focusing on the dynamics/function of the cytoplasmic RNA processing bodies called stress granules, that have been recently linked to pathogenic protein aggregation in neurodegeneration. We are utilising the LRRK2-IN-1 kinase inhibitor and LRRK2 constructs carrying disease-linked mutations to examine a role of the kinase activity in the subcellular localisation of LRRK2 under cellular stress.
Other aspects of our research are to investigate i) the properties of various alpha-synuclein alternatively spliced isoforms and ii) whether glucose metabolism is dysfunctional in PD.
Figure 1: Lewy bodies (black arrows) and Lewy neurites (white arrows) positive for phospho-alpha synuclein in a PD case. A) substantia nigra and B) cortex (cingulate gyrus).
Page last modified on 04 apr 11 10:00