- Video: Advances in Genetic Understanding of Parkinson's Disease
- GCH1 gene and Parkinson's risk
- The new Leonard Wolfson Experimental Neurology Centre (LWENC) has opened for clinical studies and trials
- LRRK2 and autophagy in fibroblasts
- LRRK2 and autophagy
- GBA and mitochondria
- Alpha-synuclein in LRRK2 brains
- α-Synucleinopathy associated with G51D SNCA mutation: A link between Parkinson’s disease and multiple system atrophy?
- Video: Parkinson's and the Genetic Revolution: From Genes to Treatments
- Public lecture: The autophagy signaling network, c-‐myc and pathology: don't mess with the cell cycle!
- Video: Brain Disease Research - Keeping You You
- Video: Degenerating Brains public symposium
- Mutations in VCP gene implicated in a number of neurodegenerative diseases
- Public lectures: new research into Alzheimer's, Parkinson's and Motor Neuron Disease
- Blog: Degenerating neurons
- Global research team discovers new Alzheimer’s risk gene
- Direct Observation of the Interconversion of Normal and Toxic Forms of a-Synuclein
- Video: The genetics of LRRK2 by Nick Wood
- Video: Parkinson's UK site visit for the Targeting LRRK2 project
- Successes of Deep Brain Stimulation for patients with Parkinson's disease
- Recordings in Parkinson's disease patients reveal details of communication between deep and superficial brain structures
- Five new Parkinson's genes identified
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...
Video: Parkinson's UK site visit for the Targeting LRRK2 project
1 November 2011
LRRK2 – pronounced lark 2 – is the most common gene associated with
Parkinson’s. A mutant form of LRRK2 can cause the death of nerve cells,
and blocking this form of LRRK2 from working can prevent this from
happening. Before we can use this knowledge to develop treatments we
need to fill in the gaps in our understanding of the role LRRK2 plays
when it’s healthy, and of the different proteins it interacts with along
the way within the nerve cell.
Figuring out how LRRK2 works and how to change this is a promising route to developing novel therapies for the treatment and ultimately cure for Parkinson’s. Although a long way off, we hope that these can ultimately be tested in the clinic to see if we can slow down or alter the progress of the condition.
Page last modified on 01 nov 11 14:21