Modelling dementia-related synaptic dysfunction in Drosophila at Royal Holloway, University of London on FindAPhD.com

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Dr Hrvoje Augustin Applications accepted all year round Self-Funded PhD Students Only

Egham United Kingdom Cell Biology Developmental Biology Genetics Molecular Biology Neuroscience Systematic Biology

About the Project

Almost a million of people in the UK live with dementia. Alzheimer’s disease (AD), dementia with Lewy bodies (DLB), and frontotemporal dementia (FTD) are the most common causes of neurodegenerative dementias. These diseases are characterised by presence of various types of aggregates of misfolded proteins in the neuronal tissue; however, evidence suggests that dysfunction and loss of the synapse might be a common pathological feature underlying the cognitive decline and memory loss in these neurodegenerative disorders.

FTD and amyotrophic lateral sclerosis (ALS) share several clinical, neuropathological and genetic features, with FTD primarily seen as a progressive brain disease, and ALS as a central and peripheral disorder affecting motoneurons controlling voluntary muscle movements. We will analyse different models of FTD/ALS in the fruit-fly Drosophila melanogaster (and, potentially, in other model species) using a plethora of genetic, molecular, imaging, computational and physiological tools to:

1. Understand the main physiological and molecular features of pathological synapses, and

2. Identify potential molecular targets for therapeutic interventions in humans

Entry Requirements:

Candidates are expected to hold (or be about to obtain) a minimum upper second class honours degree (or equivalent) in a related area / subject. Candidates with experience in electrophysiology, computational modelling or Drosophila genetics are particularly encouraged to apply.

References

1. H. Augustin et al (2019): A computational model of the escape response latency in the Giant Fiber System of Drosophila melanogaster, eNeuro.
2. H. Augustin et al (2019): Plum, a novel modulator of the action of Myoglianin on synaptic function and body size in Drosophila (bioRxiv: https://www.biorxiv.org/content/early/2018/11/06/463885).
3. 4. H. Augustin et al (2017): Reduced insulin signaling maintains electrical transmission in a neural circuit in aging flies. PLoS Biology.
4. H. Augustin et al (2017): Myostatin-like proteins proteins regulate synaptic function and neuronal morphology. Development.
5. M. K. Gorsky, S. Burnouf, O. Sofola, J. Dols, H. Augustin C et al (2017): Pseudo-acetylation of multiple sites on human Tau proteins alters Tau phosphorylation and microtubule binding and ameliorates amyloid beta toxicity. Sci Reports.
6. S. Burnouf, S. Grönke, H. Augustin, et al. (2016): Deletion of endo-genous Tau proteins is not detrimental in Drosophila, Sci Reports.
7. A. B. Ziegler, H. Augustin et al. (2016): The Amino Acid Transporter JhI-21 Coevolves with glutamate receptors, impacts NMJ physiology, and influences locomotor activity in Drosophila larvae. Sci Reports.
8. O. Sofola, F. Kerr, I. Rogers, R. Killick, H. Augustin et al. (2010): Inhibition of GSK-3 ameliorates Aβ pathology in an adult-onset Drosophila model of Alzheimer’s Disease. PLoS Genetics.
9. F. Kerr, H. Augustin et al (2009): Dietary restriction delays aging, but not neuronal dysfunction, in Drosophila models of Alzheimer's disease. Neurobiology of Aging.

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Where will I study?

Royal Holloway, University of London

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