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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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...
(Wellcome Trust Clinician Scientist)
Miratul Muqit graduated MB, ChB (Hons) from the University of Edinburgh (1991-97). He is a former Kennedy Scholar of Harvard University (2000-01) where he undertook postdoctoral studies in Mel Feany’s laboratory making Drosophila models of human neurodegenerative disease. He undertook his PhD as a MRC Clinical Training Fellow at University College London (2001-2004) jointly supervised by David Latchman and Nicholas Wood, where he studied two genes associated with early-onset Parkinson’s disease, parkin (a ubiquitin ligase) and PTEN-induced kinase 1 (PINK1).
In parallel he has trained as a clinical neurologist. He completed general medical training at the Hammersmith Hospital and hospitals affiliated to Imperial College. He then trained as a neurologist at several London hospitals including King’s College Hospital and the National Hospital for Neurology and Neurosurgery at Queen Square. He trained in movement disorders with Andrew Lees and Khailash Bhatia at the National Hospital.
In 2008 he was awarded a Wellcome Trust Intermediate Clinical Fellowship sponsored by Dario Alessi at the MRC Protein Phosphorylation Unit to investigate the molecular signaling pathways of the Parkinson’s disease associated kinases, PINK1 and LRRK2.
Page last modified on 20 mar 13 17:12