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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.

Cell Physiology Group

We are fascinated by the intimate dialogue between mitochondrial biology and cell signaling systems. How do cell signaling pathways impact on and regulate mitochondrial physiology? How do subtle changes in mitochondrial function affect the physiology of the cell? How are mitochondria in different cell types specialized to match the specialized differentiated function of the cells they inhabit? We are especially concerned to characterise the contributions of mitochondrial dysfunction to cell injury and cell death - by necrosis or apoptosis – that takes place in situations such as ischaemia, reperfusion injury and in the neurotoxicity mediated by glutamate or beta-amyloid. Another core theme again involving a complex dialogue is the mitochondrion as both a site and a target of oxidative stress and damage in disease models. 

Most of our work involves live cell fluorescence microscopy and imaging, including confocal, multiphoton and fast read-out cooled CCD instruments. All approaches have been adapted to allow the simultaneous or near simultaneous measurement of multiple variables - cytosolic calcium and mitochondrial potential, cytosolic calcium and mitochondrial calcium, NADH autofluorescence and cytosolic calcium or cytosolic magnesium and so on. We have a broad general interest in functional cellular imaging and in the development of new approaches to imaging aspects of cell function using targeted probes, GFP tagged proteins, FRET, FLIM and so on.

Interests of the lab extend through a wide range of biological problems in which mitochondria are involved - in ischaemia reperfusion injury in the heart, in the role of mitochondrial function in fertility in the mammalian egg (with John Carroll), in mitochondrial function and septic shock syndrome in liver, kidney and muscle, in mitochondrial biogenesis following exercise and training in muscle, and in mitochondrial dysfunction in beta cells in diabetes. This rather unusual breadth has had a positive influence on all our work, as resolving problems in one system invariably seems to illuminate problems with others. We have been astonished at the frequency with which a small number of basic principles are recapitulated in a wide and disparate array of models.

There is mounting evidence that PD involves mitochondrial dysfunction, both a bioenergetic deficit especially affecting complex I and a defect in quality control, with defects in autophagy. We are interested to understand the links between these, the possible roles of mitochondrial biogenesis as a protective strategy. We are also interested in the possible roles of lysosomes as a part of the autophagic machinery, as there are strong associations between lysosomal storage diseases and PD. This latter project involves collaborations with Sandip Patel and Tony Schapira (RFH).

mito potential changes with Abeta

In this movie, mitochondrial membrane potential was measured in a field of living astrocytes in culture using confocal microscopy. Cells were loaded with rhodamine 123 and potential measured as dequench (an increase in signal means mitochondrial depolarisation). Amyloid β 1-42 was applied shortly after the start of the time series. After a delay, we see a gradual progressive depolarisation of mitochondria on which are superimposed large transient depolarisations that may recover completely.

Lab website

Page last modified on 27 jan 11 15:09