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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...
(Senior Postdoctoral Research Fellow)
My interest in studying basic molecular and biochemical pathways and their dysregulation in disease has been the driving force behind the progression of my scientific career. I graduated from Edinburgh University in 2000 with a BSc Hons in Developmental Biology and was selected to undertake a PhD within the laboratory of Professor Pascal Meier at the prestigious Toby Robins Breakthrough Breast Cancer centre within the Institute of Cancer Research, London. My PhD studies focused on apoptosis pathways, specifically mechanisms of caspase activation using Drosophila melanogaster as a model organism and translating the findings into mammalian studies. During this work I identified a novel kinase involved in caspase activation. After graduating with my PhD in 2005, I undertook a short postdoctoral appointment at the School of Pharmacy in Professor Robert Harvey’s laboratory studying the Parkinson’s Disease (PD) related protein kinase PINK1. I was subsequently hired by Professor Nicholas W Wood at the UCL Institute of Neurology in 2007 to continue these studies using mammalian cell systems. I am currently a senior postdoctoral researcher employed under a strategic award from the MRC/Wellcome trust to investigate the underlying mechanisms of PD and aim to establish my own laboratory within the Institute of Neurology in the near future. At present Dr Deas supervises BSc and clinical MSc students in addition to aiding in PhD student supervision. Postdoctoral appointments under Dr Deas are currently under consideration with the relevant funding bodies
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Page last modified on 19 mar 13 16:57