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.

Dr Claire Durrant

UK Dementia Research Institute Emerging Leader 

1 George Square

Edinburgh, EH8 9JZ

Contact details

 Work: +44 (0) 131 651 1903



Personal Profile 

  • 2021 - present: UK Dementia Research Institute Emerging Leader (University of Edinburgh)
  • 2019 - 2021:     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.

Relevant Publications

Lauren VC Miller, Aamir S Mukadam, Claire S Durrant, Marina J Vaysburd, Taxiarchis Katsinelos, Benjamin J Tuck, Sophie Sanford, Olivia Sheppard, Claire Knox, Shi Cheng, Leo C James, Michael P Coleman, William A McEwan (2021) Tau assemblies do not behave like independently acting prion-like particles in mouse neural tissue. Acta Neuropathologica Comms. doi: 10.1186/s40478-021-01141-6

Kent SA, Spires-Jones TL, Durrant CS* (2020) The physiological roles of tau and Aβ: implications for Alzheimer’s disease pathology and therapeutics. Acta Neuropathologica. doi: 10.1007/s00401-020-02196-w

Durrant CS1* (2020) Preparation of Organotypic Hippocampal Slice Cultures for the Study of CNS Disease and Damage. Methods Mol Biol Clifton NJ 2143:133–144. doi: 10.1007/978-1-0716-0585-1_10

Durrant CS1, Ruscher K, Sheppard O, Coleman MP, Özen I (2020) Beta secretase 1-dependent amyloid precursor protein processing promotes excessive vascular sprouting through NOTCH3 signalling. Cell Death & Disease 11:1–15. doi: 10.1038/s41419-020-2288-4

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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