Centre for Discovery Brain Sciences
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Prof Tom Gillingwater

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.

Professor Tom Gillingwater

Professor of Anatomy

  • Hugh Robson Building
  • 15 George Square
  • Edinburgh EH8 9XD

Contact details

Personal profile

  • Chair of Anatomy (2015-present), University of Edinburgh
  • Professor of Neuroanatomy (2010-2015), 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 Royal Society of Biology (Elected 2016)

  • 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)

Research Theme


Prof. Tom Gillingwater's research briefing

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. Members of the lab 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. Currently, research efforts are focussed on: i) understanding disease mechanisms and developing new therapies for motor neuron diseases, including spinal muscular atrophy (SMA) and amyotrophic lateral sclerosis (ALS); ii) understanding common cellular and molecular mechanisms that regulate the breakdown of axonal and synaptic compartments across a range of different neurodegenerative conditions (from motor neuron disease through to Alzheimer’s disease, lysosomal storage disorders, and Huntington’s disease); and iii) developing novel imaging strategies for visualising the human nervous system in vivo.


Team members


Selected recent publications

Farrar, M.A., Park, S,B., Vucic, S., Carey, K.A., Turner, B., Gillingwater, T.H., Swoboda, K. & Kiernan, M.C. (2017) Emerging therapies and challenges in Spinal Muscular Atrophy. Annals of Neurology 81: 355-368.

Boyd, P.J., Tu, W-Y., Shorrock, H.K., Groen, E.J.N., Carter, R.N., Powis, R.A., Thomson, S.R., Thomson, S.R., Thomson, D., Graham, L.C., Motyl, A.A.L., Wishart, T.M., Highley, J.R., Morton, N.M., Becker, T., Becker, C.G., Heath, P.R. & Gillingwater, T.H. (2017) Bioenergetic status modulates motor neuron vulnerability and pathogenesis in a zebrafish model of spinal muscular atrophy. PLoS Genetics 13: e1006744.

Gillingwater, T.H. (2016) Dawn of a new therapeutic era for SMA. The Lancet 388: 2964–2965.

Hunter, G., Powis, R.A., Jones, R.A., Groen, E.J.N., Shorrock, H.K., Lane, F.M., Zheng, Y., Anderson, H., Sherman, D.L., Brophy, P.J. & Gillingwater, T.H. (2016) Restoration of SMN in Schwann cells reverses myelination defects and improves neuromuscular function in spinal muscular atrophy. Human Molecular Genetics 25: 2853-2861.

Powis, R.A., Karyka, E., Boyd, P., Come, J., Jones, R.A., Zheng, Y., Szunyogova, E., Groen, E.J.N., Hunter, G., Thomson, D., Wishart, T.M., Becker, C.G., Parson, S.H., Martinat, C., Azzouz, M. & Gillingwater, T.H. (2016) Systemic restoration of UBA1 ameliorates disease in spinal muscular atrophy. JCI Insight 1: e87908.

Somers, E., Lees, R.D., Hoban, K., Sleigh, J.N., Zhou, H., Muntoni, F., Talbot, K., Gillingwater, T.H. & Parson, S.H. (2016) Vascular defects and spinal cord hypoxia in spinal muscular atrophy. Annals of Neurology 79: 217-230.

Nicholson-Fish J.C., Kokotos A.C., Gillingwater T.H., Smillie K.J. & Cousin M.A. (2015) VAMP4 is an essential cargo molecule for activity-dependent bulk endocytosis. Neuron 88: 973-984.

Groen, E.J. & Gillingwater, T.H. (2015) UBA1: at the crossroads of ubiquitin homeostasis and neurodegeneration. Trends in Molecular Medicine 21: 622-632.

Baxter, P.S., Bell, K.F., Kaindl, A., Fricker, M., Thomson, D., Tolkovsky, A., Gillingwater, T.H. & Hardingham, G.E. (2015) Synaptic NMDA receptor activity is coupled to the transcriptional control of the glutathione system in the developing forebrain. Nature Communications 6: 6761.

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 β-catenin signalling promote spinal muscular atrophy. Journal of Clinical Investigation 124: 1821-1834.

Tom Gillingwater's publication profile