Dr Chris J H Elliott




1985 - Lecturer Biology Department, University of York
1982 - 1985 Postdoctoral research fellow University of Sussex
1980 - 1982 Postdoctoral research fellow Max Planck Institute fur Verhaltensphysiologie, Seewiesen
1980 MA Jesus College, Oxford
1977 BA Natural Sciences (Zoology) Jesus College, Oxford



My interests are in the fundamental causes of Parkinson’s disease (PD),using fly models of inherited PD to understand why (some dopaminergic)neurons die more than others. Fly models of PD are robust and recapitulatethe main features of the disease because flies share many genes withhumans. As a physiologist, I am able to use fly eyes, muscles and brains toinvestigate the first steps in the loss of function that precede cell death.



Mutations in parkin causes early onset PD (mean age of onset 32 years)and so we have been examining the effect of manipulating this gene in theyoung form of the fly, the maggot. We find that parkin maggots crawl moreslowly, and developed a novel assay to demonstrate their bradykinesia-like phenotype, in which neural function is weakened, and muscle functionremains intact. Removing oxidative stress transgenically, shows that thefundamental defects occur in ATP production, leading to disruption ofneurotransmission, and that oxidative stress is not a fundamental cause ofneuronal death in PD.


This is the most common genetic cause of PD, but the function of this gene isstill unknown. In the fly, expression of mutations that lead to PD cause a rapiddegeneration of the visual system, and loss of sight. This is most pronouncedwhen the gene is expressed in dopaminergic neurons. In this case, weobserve a spreading pathology, with non-dopaminergic neurons dying throughmitochondrial dysfunction. This is exacerbated when the metabolic load isincreased by repetitive visual stimuli.

Both these models highlight the role of mitochondrial ATP production as keydefects in PD.


Dynamic measurements of neural gain control and visual processing indrosophila models of neurological disease, The Wellcome Trust

Role of dopamine and LRRK2 mutants in the decline of vision Parkinson’s UK

Research group(s)


PhD Student Stavroula Petridi Metabolic and oxidative stress in Parkinson's disease. The Parkinson’s Disease Society (20%)
PhD Student Rebecca Furmston Synaptic physiology of Parkinson’s disease neurons
Researcher Amy Cording The physiological analysis of octopamine and tyramine in Drosophila behaviour


Available PhD research projects

Understanding the role of LRRK2 in Parkinson’s disease (2015-16)

The most common genetic cause of Parkinson’s disease (PD) is a mutation in the LRRK2 gene, G2019S. We have developed a new fly model, which exploits the homology of between fly and human. The proboscis extension response (PER)  shows a marked decline in performance with G2019S expression, but not with other mutations in LRRK2. This loss of function is most marked when G2019S is expressed in the dopaminergic neurons. It can be rescued by drug application. We will use the extensive fly genetic toolbox to test the function of G2019S as a dominant negative kinase mutation,  and to screen candidate genes which slow degeneration. We will support this by using drug application (L-DOPA, kinase inhibitors, glycolytic upregulation). This will provide a new view of LRRK2 neurophysiology in the whole organism, in a way that has not been possible in mouse models.

Dr Chris J H Elliott

Contact details

Dr Chris J H Elliott
Department of Biology (Area 9)
University of York
YO10 5DD

Tel: 01904 328654