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Professor Michael Coleman 

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Fellow Type

Senior Research Fellows,

Michael Coleman is the van Geest Professor of Neuroscience in the Department of Clinical Neurosciences, University of Cambridge, and joined Churchill College, Cambridge, as a Senior Research Fellow. His research groups studies mechanisms of axon degeneration and synapse loss, in particular the mechanism of programmed axon death (or Wallerian degeneration) that can be activated by axon injury, gene mutation, toxins and viruses. When activated specifically, this mechanism can be fully blocked by removing the gene for SARM1, one of a number of observations that has led to SARM1 becoming an important drug target. In addition to evidence in animal models of involvement in many neurodegenerative disorders, his group and their collaborators have used human genetics to establish roles in some types of polyneuropathy and motor neuron disease.

Professor Coleman previously led research groups in this field at the Babraham Institute, Cambridge, Cologne, Germany and Oxford. He leads a Wellcome Trust Collaboration Award project on programmed axon death in human disease together with groups at UCL, Oxford and Baltimore, he cofounded the Axon Degeneration Workshop series which has run since 2006, he has served on grant review boards for Alzheimer’s Research UK, BBSRC, DFG, ALS Association and AriSLA, and was a joint winner of the Lalji Family ALS Award in 2021. Professor Coleman has a growing interest in coaching and mentoring of academics, including leading an ECR peer mentoring group for Alzheimer’s Research UK. He is a strong advocate of efforts to modernise and improve the culture of academic research in this and other ways.

Lab website and blog:

Twitter: @Lab_Coleman

Key Publications

Loreto, A., et al (2021) “Neurotoxin-mediated potent activation of the axon degeneration regulator SARM1”. eLife 10: e72823.

Gilley, J., et al (2021) “Enrichment of SARM1 alleles encoding variants with constitutively hyperactive NADase in patients with ALS and other motor nerve disorders”. eLife 10: e70905

Coleman, M.P. and Höke, A. (2020) Programmed axon degeneration: from mouse to mechanism to medicine. Nat Rev Neurosci 21: 183-196.

Lukacs, M.*, Gilley, J.*, Zhu, Y*, et al (2019).  Severe biallelic loss-of-function mutations in NMNAT2 in two fetuses with fetal akinesia deformation sequence. Exp Neurol. 320: 112961

Huppke, P., et al (2019). Homozygous NMNAT2 mutation in sisters with polyneuropathy and erythromelalgia. Exp Neurol. 320: 112958

*Di Stefano, M., *Nascimento-Ferreira, I., et al (2014). A rise in NAD precursor nicotinamide mononucleotide (NMN) after injury promotes axon degeneration. Cell Death Diff. 22: 731-742

Gilley, J., et al (2010) Endogenous Nmnat2 is an essential survival factor for maintenance of healthy axons.  PLOS Biol 8: (1) e1000300

Mack, T.G.A., et al (2001) Wallerian degeneration of injured axons and synapses is delayed by a Ube4b/Nmnat chimeric gene   Nature Neuroscience  4: 1199-1206