Centre for Discovery Brain Sciences
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Prof Tara Spires-Jones

Our research focuses on the mechanisms and reversibility of synapse degeneration in Alzheimer’s disease, other degenerative brain diseases, and ageing.

Professor Tara Spires-Jones

Personal Chair of Neurodegeneration; Deputy Director of the Centre for Discovery Brain Sciences

  • 1 George Square
  • Edinburgh, EH8 9JZ

Contact details

Personal profile

  • 2017 - Present: Professor of Neurodegeneration, UK Dementia Research Institute Programme Lead, Deputy Director of the Centre for Discovery Brain Sciences; University of Edinburgh (funded by UofE, ERC Consolidator Award, and the UK Dementia Research Instutute)
  • 2016 - 2017: Interim Director, Centre for Cognitive and Neural Systems; University of Edinburgh (funded by UofE and ERC Consolidator Award)
  • 2013 - 2017: Reader and Chancellor’s Fellow; University of Edinburgh
  • 2011 - 2013: Assistant Professor; Massachusetts General Hospital/ Harvard Medical School
  • 2006 - 2011: Instructor; Massachusetts General Hospital/ Harvard Medical School
  • 2004 - 2006: Research Fellow Neurology; Massachusetts General Hospital/ Harvard Medical School
  • 2000 - 2004: DPhil Neuroscience; University of Oxford

Research Theme

Research

Tara Spires-Jones’ research focuses on the mechanisms and reversibility of neurodegeneration in Alzheimer’s disease, other degenerative brain diseases, and ageing.  Working with a vibrant group of researchers, she is trying to understand why synapses and neurons become dysfunctional and die in these diseases in order to develop effective therapeutic strategies. Her work has shown that soluble forms of the pathological proteins amyloid beta and tau contribute to synapse degeneration, and that lowering levels of these proteins can prevent and reverse phenotypes in model systems. Further, she has pioneered high-resolution imaging techniques in human post-mortem brain and found evidence that these proteins accumulate in synapses in human disease.  Tara Spires-Jones has published over 100 peer reviewed papers which have been cited over 13,000 times. 

In addition to her research, Prof Spires-Jones is passionate about communicating scientific findings to the public and policy makers; increasing the rigour and reproducibility in translational neuroscience; promoting inclusivity and diversity in science; and supporting career development of neuroscientists.  She is founding editor of the translational neuroscience journal Brain Communications, a member of the Board of Reviewing Editors at Science, Section Editor a the European Journal of Neuroscience, and is on the editorial boards of Neuron and Cell Reports. She was also a founding member of the FENS-Kavli Network of Excellence, which works to promote the future of European Neuroscience. She served as a member of the Scottish Science Advisory Council from 2016-2019 advising the Scottish Government on science policy, and in 2018 was elected as a term Member of the European Dana Alliance of the Brain promoting public engagement with neuroscience. 

Prior to moving to Scotland in 2013, Tara Spires-Jones ran a group studying Alzheimer’s disease pathogenesis with an emphasis on synaptic pathology at Massachusetts General Hospital (MGH) and Harvard Medical School, where she was Instructor from 2006-2011 and Assistant Professor from 2011-2013.  She completed graduate training (MSc and DPhil) at the University of Oxford from 1999-2003, and undergraduate training at the University of Texas at Austin from 1994-1999. 

Funding

Team members

Collaborations

Selected Publications

Pickett, E. K., Herrmann, A. G., McQueen, J., Abt, K., Dando, O., Tulloch, J., Jain, P., Dunnett, S., Sohrabi, S., Fjeldstad, M. P., Calkin, W., Murison, L., Jackson, R. J., Tzioras, M., Stevenson, A., d’Orange, M., Hooley, M., Davies, C., Colom-Cadena, M., Anton-Fernandez, A., King, D., Oren, I., Rose, J., McKenzie, C.-A., Allison, E., Smith, C., Hardt, O., Henstridge, C. M., Hardingham, G. E., & Spires-Jones, T. L. (2019). Amyloid Beta and Tau Cooperate to Cause Reversible Behavioral and Transcriptional  Deficits in a Model of Alzheimer’s Disease. Cell Reports, 29(11), 3592-3604.e5. https://doi.org/10.1016/j.celrep.2019.11.044 

Henstridge, C. M., Hyman, B. T., & Spires-Jones, T. L. (2019). Beyond the neuron-cellular interactions early in Alzheimer disease pathogenesis. Nature Reviews. Neuroscience, 20(2), 94–108. https://doi.org/10.1038/s41583-018-0113-1 

Hesse, R., Hurtado, M. L., Jackson, R. J., Eaton, S. L., Herrmann, A. G., Colom-Cadena, M., Tzioras, M., King, D., Rose, J., Tulloch, J., McKenzie, C.-A., Smith, C., Henstridge, C. M., Lamont, D., Wishart, T. M., & Spires-Jones, T. L. (2019). Comparative profiling of the synaptic proteome from Alzheimer’s disease patients  with focus on the APOE genotype. Acta Neuropathologica Communications, 7(1), 214. https://doi.org/10.1186/s40478-019-0847-7 

Tzioras, M., Davies, C., Newman, A., Jackson, R., & Spires-Jones, T. L. (2019). Invited Review: APOE at the interface of inflammation, neurodegeneration and  pathological protein spread in Alzheimer’s disease. Neuropathology and Applied Neurobiology, 45(4), 327–346. https://doi.org/10.1111/nan.12529 

Jackson, R. J., Rose, J., Tulloch, J., Henstridge, C., Smith, C., & Spires-Jones, T. L. (2019). Clusterin accumulates in synapses in Alzheimer’s disease and is increased in  apolipoprotein E4 carriers. Brain Communications, 1(1), fcz003. https://doi.org/10.1093/braincomms/fcz003 

Pickett, E. K., Rose, J., McCrory, C., McKenzie, C.-A., King, D., Smith, C., Gillingwater, T. H., Henstridge, C. M., & Spires-Jones, T. L. (2018). Region-specific depletion of synaptic mitochondria in the brains of patients with  Alzheimer’s disease. Acta Neuropathologica, 136(5), 747–757. https://doi.org/10.1007/s00401-018-1903-2 

Henstridge CM, Sideris DI, Carroll E, Rotariu S, Salomonsson S, Tzioras M, McKenzie CA, Smith C, von Arnim CAF, Ludolph AC, Lulé D, Leighton D, Warner J, Cleary E, Newton J, Swingler R, Chandran S, Gillingwater TH, Abrahams S, Spires-Jones TL. Synapse loss in the prefrontal cortex is associated with cognitive decline in amyotrophic lateral sclerosis. Acta Neuropathol. 2017 Dec 22. doi: 10.1007/s00401-017-1797-4.

Colom-Cadena M, Pegueroles J, Herrmann AG, Henstridge CM, Muñoz L, Querol-Vilaseca M, Martín-Paniello CS, Luque-Cabecerans J, Clarimon J, Belbin O,  Núñez-Llaves R, Blesa R, Smith C, McKenzie CA, Frosch MP, Roe A, Fortea J, Andilla J, Loza-Alvarez P, Gelpi E, Hyman BT, Spires-Jones TL*, Lleó A*. Synaptic phosphorylated α-synuclein in dementia with Lewy bodies. Brain. 2017 Dec 1;140(12):3204-3214. doi: 10.1093/brain/awx275. PubMed PMID: 29177 27. * equal contributions

Jackson RJ, Rudinskiy N, Herrmann AG, Croft S, Kim JM, Petrova V, Ramos-Rodriguez JJ, Pitstick R, Wegmann S, Garcia-Alloza M, Carlson GA, Hyman BT, Spires-Jones TL. Human tau increases amyloid β plaque size but not amyloidβ-mediated synapse loss in a novel mouse model of Alzheimer's disease. Eur J Neurosci. 2016 Dec;44(12):3056-3066. doi: 10.1111/ejn.13442.

Spires-Jones TL, Hyman BT. The intersection of amyloid beta and tau at synapses in Alzheimer's disease. Neuron. 2014 May 21;82(4):756-71. dos: 10.1016/j.neuron.2014.05.004. 

Kay KR, Smith C, Wright AK, Serrano-Pozo A, Pooler AM, Koffie R, Bastin ME, Bak TH, Abrahams S, Kopeikina KJ, McGuone D, Frosch MP, Gillingwater TH, Hyman BT, Spires-Jones TL. Studying synapses in human brain with array tomography and electron microscopy. Nat Protoc. 2013;8(7):1366-80. doi: 10.1038/nprot.2013.078.

Information for students:

Willingness to discuss research projects with undergraduate and postgraduate students: YES - please click here