Claire Durrant (née Harwell)
My work aims to determine whether loss of normal tau function contributes to synaptic pathology in Alzheimer’s disease and related disorders.
- 2019 - present: Race Against Dementia Dyson Fellow, Centre for Discovery Brain Sciences, University of Edinburgh
- 2016 - 2019: Postdoctoral Researcher (funded by Alzheimer’s Research UK), Department of Clinical Neurosciences, University of Cambridge
- 2013 - 2016: PhD (funded by Alzheimer’s Research UK), The Babraham Institute, University of Cambridge
- 2010 - 2013, BA Natural Sciences, Clare College, University of Cambridge
Synapse loss is the best correlate of clinical outcome in Alzheimer’s disease, so protecting these vital structures is a key focus for the development of therapeutics to treat or prevent dementia. My work aims to determine whether loss of normal tau function contributes to synaptic pathology in Alzheimer’s disease and related disorders. By examining the physiological role of tau at the synapse and how this changes during disease, I hope to identify potential mechanisms for protecting synapses. I specialise in organotypic brain slice cultures and translational research using both human and murine tissue.
- Olivia Sheppard, Michael P. Coleman, Claire S. Durrant (2019) Lipopolysaccharide-induced neuroinflammation induces presynaptic disruption through a direct action on brain tissue involving microglia-derived interleukin 1 beta. Journal of Neuroinflammation (1),106
- Robert Adalbert, Stefan Milde, Claire Durrant, Kunie Ando, Virginie Stygelbout, Zehra Yilmaz, Stacey Gould, Jean-Pierre Brion, Michael P. Coleman (2018) Interaction between a MAPT variant causing frontotemporal dementia and mutant APP affects axonal transport. Neurobiology of Aging 68 (68 –75)
- Harwell, C.S & Coleman M.P (2016) Synaptophysin depletion and intraneuronal Aβ in organotypic hippocampal slice cultures from huAPP transgenic mice. Molecular Neurodegeneration 11 (1), 44
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