Dr Ryan West
Neuroscience, School of Medicine and Population Health
+44 114 222 2239
Full contact details
Neuroscience, School of Medicine and Population Health
Sheffield Institute for Translational Neuroscience (SITraN)
385a Glossop Road
2019 – Present: SITraN Fellow and Alzheimer’s Society Fellow (SITraN, University of Sheffield)
2018 – 2019: Alzheimer’s Society Junior Fellow (University of Manchester)
2015 – 2018: Postdoctoral Research Associate (University of York)
2013-2015: Centre for Chronic Diseases and Disorders Wellcome Trust funded “Discipline hopping” Fellow (University of York)
Following an Industrial placement year at Eli Lilly, working on murine models of Parkinson’s Disease I moved to York in 2010 to do my PhD in the lab of Sean Sweeney, characterising a Drosophila model of Frontotemporal Dementia associated with the CHM2BIntron5 mutation. After my PhD I remained in York as Wellcome trust funded “discipline hopping” fellow looking at visual disturbances in Parkinson’s disease and then as a post-doc continuing my work on CHMP2B and the role of POSH as a JNK scaffold in FTD. In 2017 I was awarded an Alzheimer’s Society Fellowship and moved to Manchester in 2018. At the end of October 2019, I moved to SITraN to continue my Alzheimer’s Society Fellowship and take up a position as a SITraN Fellow. Here I am establishing Drosophila facilities within SITraN and continuing my work on Drosophila models of neurodegeneration.
- Research interests
My research looks to use Drosophila melanogaster (fruit flies) as a powerful genetic model organism to dissect the molecular mechanisms contributing to neurodegenerative diseases including dementia, motor neurone disease and Parkinson’s disease. My primary research focuses on two overlapping neurodegenerative disorders, Frontotemporal Dementia (FTD) and Motor Neurone Disease (MND). I am particularly interested in how dipeptide-repeats associated with the disease causing hexanucleotide expansion within the C9orf72 gene contribute towards neurodegeneration. In the lab we have a number of Drosophila models of both FTD and MND including C9orf72 related DPRs, C9orf72 pure repeat models and models of CHMP2B, VCP and TDP-43 related disease. I am also interested in how we can use Drosophila as part of a translational pipeline both to understand the molecular mechanisms of disease and as part of a drug-screening strategy.
- Dissecting the role of POSH as a JNK Scaffold in Frontotemporal Dementia
- How physiologically relevant repeat length dipeptide-repeats interact in vivo to mediate neurodegeneration
- UDCA as a Neuroprotective compound in Drosophila models of Neurodegeneration
- Drosophila as a model for Drug Screens in Neurodegenerative Diseases
- Identification and Monitoring of Nucleotide Repeat Expansions Using Southern Blotting in Drosophila Models of C9orf72 Motor Neuron Disease and Frontotemporal Dementia. Bio-protocol, 12(10).
- Lessons learned from CHMP2B, implications for frontotemporal dementia and amyotrophic lateral sclerosis. Neurobiology of Disease, 147. View this article in WRRO
- Co-expression of C9orf72 related dipeptide-repeats over 1000 repeat units reveals age- and combination-specific phenotypic profiles in Drosophila. Acta Neuropathologica Communications, 8.
- Neuroprotective activity of ursodeoxycholic acid in CHMP2B Intron5 models of frontotemporal dementia. Neurobiology of Disease, 144.
- Ik2/TBK1 and Hook/Dynein, an adaptor complex for early endosome transport, are genetic modifiers of FTD-associated mutant CHMP2B toxicity in Drosophila. Scientific Reports, 10(1).
- Autism sensory dysfunction in an evolutionarily conserved system. Proceedings of the Royal Society B: Biological Sciences, 285(1893). View this article in WRRO
- Sphingolipids regulate neuromuscular synapse structure and function in Drosophila. Journal of Comparative Neurology, 526(13), 1995-2009. View this article in WRRO
- Abnormal visual gain control and excitotoxicity in early-onset Parkinson’s disease Drosophila models. Journal of Neurophysiology, 119(3), 957-970.
- The pro-apoptotic JNK scaffold POSH/SH3RF1 mediates CHMP2BIntron5-associated toxicity in animal models of frontotemporal dementia. Human Molecular Genetics, 27(8), 1382-1395. View this article in WRRO
- A perceptive plus in Parkinson's disease. Movement Disorders, 33(2), 248-248. View this article in WRRO
- Identification of dietary alanine toxicity and trafficking dysfunction in a Drosophilamodel of hereditary sensory and autonomic neuropathy type 1. Human Molecular Genetics, 24(24), 6899-6909.
- Classification of Parkinson’s Disease Genotypes in Drosophila Using Spatiotemporal Profiling of Vision. Scientific Reports, 5(1).
- Eyeing up Drosophila models of frontotemporal dementia: identifying conserved mechanisms in disease pathology. Future Neurology, 10(6), 507-510.
- Binding partners of the kinase domains in Drosophila obscurin and their effect on the structure of the flight muscle. Journal of Cell Science, 128(18), 3386-3397.
- Rab8, POSH, and TAK1 regulate synaptic growth in a Drosophila model of frontotemporal dementia. Journal of Cell Biology, 208(7), 931-947.
- Neurophysiology ofDrosophilaModels of Parkinson’s Disease. Parkinson's Disease, 2015, 1-11.
- Oxidative stress and autophagy. Autophagy, 8(2), 284-285.
- Modeling C9orf72-Related Frontotemporal Dementia and Amyotrophic Lateral Sclerosis in Drosophila. Frontiers in Cellular Neuroscience, 15.
- Reactive oxygen species regulate activity-dependent neuronal plasticity in Drosophila. eLife, 7.
- Autism sensory dysfunction in an evolutionarily conserved system, Cold Spring Harbor Laboratory.
- Research group
- Duncan Garner (Dipeptide Repeat Interactions In Drosophila Models of C9orf72 Frontotemporal Dementia and Motor Neurone Disease)