Prof Tom Gillingwater

Thomas Gillingwater
  • Prof Tom Gillingwater
  • Professor of Neuroanatomy
  • Hugh Robson Building 15 George Square Edinburgh EH8 9XD
  • Work: +44 (0)131 650 3724

Personal profile

  • Professor of Neuroanatomy (2010-present), University of Edinburgh
  • Senior Lecturer in Anatomy (2008-2010), University of Edinburgh
  • Lecturer in Anatomy (2004-2008), University of Edinburgh
  • MBA, University of Edinburgh (2006)
  • PhD in Neuroscience, University of Edinburgh (2001)
  • BSc (Hons) in Human Biology (Anatomy), University of Leeds (1998)
  • Editor-in-Chief: Journal of Anatomy (2011-present; Receiving Editor 2008-2011)
  • Academic Editor: PLoS One (2011- present)
  • Fellow of the Anatomical Society (Elected 2012)
  • Fellow of the Royal Microscopical Society (Elected 2005)
  • Member of the Institute of Directors (Elected 2011)
  • Teaching Responsibilities: Gross Human Anatomy and Neuroanatomy (MBChB & MSc Human Anatomy) and Course Director for Anatomy & Pathology 2 (BSc Medical Sciences)


Electron micrograph of a control neuromuscular junction

Figure 1: Electron micrograph of a control neuromuscular junction

Research in the Gillingwater lab focuses on understanding cellular and molecular mechanisms that regulate the form and function of the nervous system in health and disease. At present we are undertaking projects investigating:

i) mechanisms underlying pathogenesis of the childhood motor neurone disease Spinal Muscular Atrophy (SMA) ii) common mechanisms regulating degeneration of synaptic connections across a range of different neurodegenerative conditions (from Alzheimer's disease and Huntington's disease through to lysosomal storage disorders and motor neurone diseases) iii) novel neuroprotective treatment strategies that can delay or prevent neurodegenerative disease iv) novel in vitro screening platforms for modeling neurodegenerative diseases using human stem cells (iPSCs) v) the influence of axon-glial interactions for stability of the peripheral nervous system

We routinely combine quantitative imaging (e.g. confocal and electron microscopy) and molecular biology techniques (e.g. proteomics and microarray screens) to study the structure and function of the central and peripheral nervous systems, both in vivo and in vitro.

Further information on Professor Gillingwater's spin out company, NeuroORG Business Consulting Ltd, is available on the website;


  • Anatomical Society
  • Biotechnology and Biological Sciences Research Council (BBSRC)
  • Birth Defects Foundation (BDF) Newlife
  • Euan MacDonald Centre for Motor Neurone Disease Research
  • GlaxoSmithKline plc (GSK)
  • MND Scotland
  • Muscular Dystrophy Campaign
  • SMA Trust
  • Sylvia Aitken Charitable Trust
  • Wellcome Trust
  • AxonomiX EU Network

Team members

  • Ann Wright
  • Arwin Aghamaleky
  • Chantal Mutsaers
  • Derek Thomson
  • Eilidh Somers
  • Gillian Hamilton
  • Ines Amorim
  • Rachael Powis
  • Sarah Roche
  • Sophie Thomson
  • Ewout Groen


  • J Cooper - Institute of Psychiatry, King’s College London
  • M Freeman - University of Massachusetts
  • D Lamont - Dundee University
  • I Robinson - University of Plymouth
  • K Talbot - University of Oxford
  • J Tyynelä - University of Helsinki
  • B Wirth - University of Cologne
Gillingwater book covers

Selected recent publications

Wishart, T.M., Mutsaers, C.A., Riessland, M., Reimer, M.R., Hunter, G., Hannam, M.L., Eaton, S., Fuller, H.R., Roche, S.L., Somers, E., Morse, R., Young, P.J., Lamont, D.J., Hammerschmidt, M., Joshi, A., Hohenstein, P., Morris, G.E., Parson, S.H., Skehel, P.A., Becker, T., Robinson, I.M., Becker, C.G., Wirth, B. & Gillingwater, T.H. (2014) Dysregulation of ubiquitin homeostasis and ?-catenin signalling promote spinal muscular atrophy. Journal of Clinical Investigation In Press.

Hunter, G., Aghamaleky Sarvestany, A., Roche, S.L., Symes, R.C. & Gillingwater, T.H. (2014) SMN-dependent intrinsic defects in Schwann cells in mouse models of spinal muscular atrophy. Human Molecular Genetics In Press.

Pettit, L.D., Bastin, M.E., Smith, C., Bak, T.H., Gillingwater, T.H. & Abrahams, S. (2013) Executive deficits, not processing speed relates to abnormalities in distinct prefrontal tracts in amyotrophic lateral sclerosis. Brain 136: 3290-3304.

Kay, K., Smith, C., Wright, A.K., Serrano-Pozo, A., Pooler, A., Koffie, R., Bastin, M.E., Bak, T.H., Abrahams, S., Kopeikina, K.J., Frosch, M., Gillingwater, T.H., Hyman, B.T. & Spires-Jones, T.L. (2013) Studying synapses in human brain with array tomography and electron microscopy. Nature Protocols 8: 1366-1380.

Hamilton, G. & Gillingwater, T.H. (2013) Spinal muscular atrophy: going beyond the motor neuron. Trends in Molecular Medicine 19: 40-50.

Wishart, T.M., Rooney, T., Lamont, D.J., Wright, A.K., Morton, A.J., Jackson, M., Freeman, M.R. & Gillingwater, T.H. (2012) Combining Comparative Proteomics and Molecular Genetics Uncovers Regulators of Synaptic and Axonal Stability and Degeneration In Vivo. PLoS Genetics 8: e1002936.

Avery, M., Rooney, T.M., Pandya, J.D., Wishart, T.M., Gillingwater, T.H., Geddes, J.W., Sullivan, P. & Freeman, M.R. (2012) WldS prevents axon degeneration through increased mitochondrial flux and enhanced mitochondrial Ca2+ buffering. Current Biology 22: 596-600.

Mutsaers, C.A., Wishart, T.M., Lamont, D.J., Riessland, M., Comley, L.H., Murray, L.M., Parson, S.H., Lochmüller, H., Wirth, B., Talbot, K. & Gillingwater, T.H. (2011) Reversible molecular pathology of skeletal muscle in spinal muscular atrophy. Human Molecular Genetics 20: 4334-4344.

Comley, L.H., Fuller, H.R., Wishart, T.M., Mutsaers, C.A., Thomson, D., Wright, A.K., Ribchester, R.R., Morris, G.E., Parson, S.H., Horsburgh, K. & Gillingwater, T.H. (2011) ApoE isoform-specific regulation of regeneration in the peripheral nervous system. Human Molecular Genetics 20: 2406-2421.

Patani, R., Hollins, A.J., Wishart, T.M., Puddifoot, C.A., Alvarez, S., de Lera, A.R., Wyllie, D.J.A., Compston, D.A.S., Pedersen, R.A., Gillingwater, T.H., Hardingham, G.E., Allen, N.D & Chandran, S. (2011) Retinoid independent motor neurogenesis from human embryonic stem cells reveals a medial columnar ground state. Nature Communications 2: 214.

Wishart, T.M., Huang, J, P-W., Murray, L.M., Lamont, D.J., Mutsaers, C.A., Ross, J., Geldsetzer, P., Ansorge, O., Talbot, K., Parson, S.H. & Gillingwater, T.H. (2010) SMN deficiency disrupts brain development in a mouse model of severe spinal muscular atrophy. Human Molecular Genetics 19: 4216-4228.

van der Pluijm, I., de Waard, M.C., Zuiderveen-Borgesius, N., Comley, L.H., Rijksen, Y., Ridwan, Y., Zondag, G., Hoeijmakers, J., Elgersma, Y., Gillingwater, T.H. & Jaarsma, D. (2010) Age-related motor neuron degeneration in DNA repair-deficient Ercc1 mice. Acta Neuropathologica 120: 461-475.

Murray, L.M., Lee, S., Baumer, D., Parson, S.H., Talbot, K. & Gillingwater, T.H. (2010) Pre-symptomatic development of lower motor neuron connectivity in a mouse model of severe spinal muscular atrophy. Human Molecular Genetics 19: 420-433.

Bäumer, D., Lee, S., Nicholson, G., Davies, J.L., Parkinson, N.J., Murray, L.M., Gillingwater, T.H., Ansorge, O., Davies, K.E. & Talbot, K. (2009) Alternative splicing events are a late feature of pathology in a mouse model of spinal muscular atrophy. PLoS Genetics 5: e1000773.

Kielar, C., Wishart, T.M., Palmer, A., Dihanich, S., Wong, A.M., Macauley, S.L., Chun, C-H., Sands, M.S., Pearce, D., Cooper, J.D. & Gillingwater, T.H. (2009) Molecular correlates of axonal and synaptic pathology in mouse models of Batten disease. Human Molecular Genetics 18: 4066-4080.

Wishart, T.M., Pemberton, H.N., James, S.R., McCabe, C.J. & Gillingwater, T.H. (2008) Modified cell cycle status in a mouse model of altered neuronal vulnerability (Wallerian Degeneration Slow; Wlds). Genome Biology 9(6): R101.

Murray, L.M., Comley, L.H., Thomson, D., Parkinson, N., Talbot, K. & Gillingwater, T.H. (2008) Selective vulnerability of motor neurons and dissociation of pre- and post-synaptic pathology at the neuromuscular junction in mouse models of spinal muscular atrophy. Human Molecular Genetics 17: 949-962.

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