Colin Crawford

My research explores the reparative function of the immune system following stroke and strategies to pharmacologically augmented this process to improve long-term cognitive and motor function.

Dr Colin Crawford

Research Fellow - McColl Lab

Chancellor's Building

49 Little France Crescent

Edinburgh, EH16 4SB

Contact details

 Work: +44 (0) 131 242 6293


 Web: McColl Research Group


Personal profile

  • 2021 - present:  Research Fellow - McColl lab
  • 2017 - 2021:  PhD in Neuroimmunology at the University of Glasgow 
  • 2016 - 2017:  MRes in Biomedical Sciences at the University of Glasgow
  • 2012 - 2016:  BSc (Hons) in Applied Pharmacology at Queen Margaret University, Edinburgh


Stroke is a leading cause of death and carries long-term disability for survivors in the form of motor and cognitive function deficits. Limited therapeutic options are available to only a small proportion of stroke patients due to the narrow time frame available for administration; therefore, novel therapeutics that can be administered to a broader range of patients and target functional recovery in stroke are a major research focus within the field. The immune system plays a key role in the pathology of stroke but is essential for subsequent tissue repair. In the McColl group, my work explores how the reparative function of the immune system is regulated and may be pharmacologically augmented to improve long-term cognitive and motor function after stroke. At the cellular level, we are interested in how plasticity of neuronal connections allows for the partial recovery in function after stroke and we are investigating the role of myeloid cells in this re-wiring process. Amplifying the pro-reparative function of myeloid cells is a promising future therapeutic approach to stroke treatment.

Relevant Publications 

Crawford, C.L., Antoniou, C., Komarek, L., Schultz, V., Donald, C.L., Montague, P., Barnett, S.C., Linington, C., Willison, H.J., Kohl, A., Coleman, M.P., Edgar, J.M. (2022). “SARM1 depletion slows axon degeneration in a CNS model of neurotropic viral infection”. Frontiers in Molecular Neuroscience, DOI:

McGonigal, R., Campbell, C.I., Barrie, J.A., Yao, D., Cunningham, M.E., Crawford, C.L., Rinaldi, S., Rowan, E.G., Willison, H.J. (2022). “Schwann cell nodal membrane disruption triggers bystander axonal degeneration in a Guillain-Barré syndrome mouse model”. Journal of Clinical Investigation, DOI:

Schultz, V., Barrie, J.A., Donald, C.L., Crawford, C.L., Mullin, M., Anderson, T.J., Solomon, T., Barnett, S.C., Linington, C., Kohl, A., Willison, H.J., Edgar, J.M. (2021). “Oligodendrocytes are susceptible to Zika virus infection in a mouse model of perinatal exposure: implications for CNS complications”. Glia, DOI:

Bijland, S., Thomson, G., Euston, M., Michail, K., Thümmler, K., Mücklisch, S., Crawford, C L., Barnett, S.C., McLaughlin, M., Anderson, T.J., Linington, C., Brown, E.R., Kalkman, E.R., Edgar, J.M. (2019). “An in vitro model for studying CNS white matter: functional properties and experimental approaches”. F1000Research, DOI: