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chromosome 22q deletion

Parkinson's chromosome deletion linked to other genetic disorders

Researchers, led by BRC-supported Professor Nicholas Wood, UCL Institute of Neurology, have made a breakthrough in their understanding of Parkinson’s disease after they discovered a chromosome deletion linked to Parkinson’s disease and other genetic disorders. More...

Prof John Hardy

Prof John Hardy is the first UK winner of $3m Breakthrough Prize in Life Sciences

Professor John Hardy (UCL Institute of Neurology) has been awarded the $3 million Breakthrough Prize in Life Sciences for his pioneering research into the genetic causes of Alzheimer’s disease, other forms of dementia and Parkinson’s disease. More...

John Hardy, PhD, right, accepted the 2015 Robert A. Pritzker Prize from MJFF VP Brian Fiske, PhD, and Michael J. Fox on April 15.

John Hardy awarded 2015 Robert A. Pritzker Prize for Leadership in Parkinson's Research

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 - Prof Nicholas Wood - Advances in Genetic Understanding of Parkinson's Disease.

Video: Advances in Genetic Understanding of Parkinson's Disease

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...

Pedigrees and I-FP-CIT SPECT scan images of the four families with GCH1 mutations involved in this study.

GCH1 gene and Parkinson's risk

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.

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.

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).

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).

Lab website

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