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Sophie Payne

PhD (Neuroscience) BSc Hons

Research Fellow, Bionics Institute

P: +61 3 9667 7599
F: +61 3 9667 7542
E: spayne@bionicsinstitute.org

Dr Sophie Payne started working at the Bionics Institute in 2015 to work on a project investigating ‘Neuromodulation of the vagus nerve (VN) for the treatment of inflammatory bowel disease’ that is funded by the Defence Advanced Research Project’s Agency (DARPA), an agency of the US Department of Defence. Sophie coordinates a large team that includes bio-engineers (Bionics Institute), neuroscientists (Florey Institute of Neuroscience and Mental Health, The University of Melbourne) and gastroenterologist surgeons (Austin Health) that are working together to develop a bionic solution to inflammatory bowel diseases, such as Crohn’s disease and ulcerative colitis.

A specific focus of Sophie’s work at the Bionic Institute is to develop a device that acts as a biomarker and detects the degree of inflammation in the gut, while the second key aim is to develop and optimise a device for the stimulation of the vagus nerve that best reduces symptoms of the inflammatory disease. Together, it is anticipated that these devices will be combined to form a closed loop system for the continual detection and treatment (through VN stimulation) of inflammatory bowel disease in human patients. A highlight for Sophie has been close collaboration  with a leading edge, multi-disciplined  team that has rapidly developed a potential biomarker of gut inflammation, thereby swiftly moving the project closer to clinical trials.

Sophie was also awarded a project grant (Early Career Research internal grant scheme, Melbourne University) that will fund a project that continues her research interest in myelinating glia in the central nervous system. This project will assess changes to myelin and node morphology in the optic nerve following chronic blindness, and therefore further the understanding of the model.

Prior to joining the Bionics Institute, Sophie completed her PhD at the University of Western Australia (2009-2012), where she investigated long term effects of injury to the optic nerve on myelinating glia. In 2012, Sophie started her first post doctorate position with Professor Janet Keast at the University of Melbourne, assessing regeneration and repair of the autonomic nervous system.

Research fields of interest

  • Medical Bionics

  • Autonomic nervous system

  • Inflammatory diseases

  • Multiple sclerosis and remyelination in the central nervous

Research projects

  • Neuromodulation of the vagus nerve for the treatment of inflammatory bowel disease (funded by DARPA)

  • Myelin sheath integrity and node morphology of the optic nerve following blindness (funded by the Early Career Research Scheme, University of Melbourne)

Publications

  1. Payne S. C, Belleville P. J, Keast J. R. Regeneration of sensory but not motor axons following visceral nerve injury. April 2015. Exp Neurol. 266; 127-142
    http://www.ncbi.nlm.nih.gov/pubmed/25725351

  2. Wong A. W, Yeung J. K, Payne S. C, Keast J. R, Osborne P. Neurite outgrowth in normal and injured primary sensory neurons reveals different regulation by nerve growth factor (NGF) and Artemin. March 2015. Molecular and Cellular Neuroscience. 65: 125-134
    http://www.ncbi.nlm.nih.gov/pubmed/25752731

  3. Forrest S. L, Payne S. C, Keast J. R, Osborne P. B. Peripheral injury of pelvic visceral sensory nerves alters GFRα (GDNF family receptor alpha) localization in sensory and autonomic pathways of the sacral spinal cord. April 2015. Frontiers in Neuroanatomy.
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4392586

  4. Szymanski C.R, Chiha W, Morellini N, Cummins N, Bartlett C.A, O’Hare Doig R.L, Savigni D.L, Payne S.C, Harvey A.R, Dunlop S.A, Fitzgerald M. Paranode Abnormalities and Oxidative Stress in Optic Nerve Vulnerable to Secondary Degeneration: Modulation by 670 nm Light Treatment. June 2013. PLoS ONE. 19;8(6): e66448
    http://www.ncbi.nlm.nih.gov/pubmed/23840470

  5. Payne S.C, Bartlett C.A, Savigni D.L, Harvey A.R, Dunlop S.A, Fitzgerald M. Early proliferation does not prevent the loss of oligodendrocyte progenitor cells during the chronic phase of secondary degeneration in a CNS white matter tract. PLoS ONE. June 2013. 11;8(6): e65710
    http://www.ncbi.nlm.nih.gov/pubmed/23776532

  6. Payne S.C, Bartlett C.A, Harvey A.R, Dunlop S.A, Fitzgerald M. Myelin sheath decompaction, axon swelling and functional loss during chronic secondary degeneration in rat optic nerve. Invest Opthalmol Vis Sci. September 2012. 4; 53(10):6093-101
    http://www.ncbi.nlm.nih.gov/pubmed/22879411

  7. Payne S.C, Bartlett C.A, Harvey A.R, Dunlop S.A, Fitzgerald M. Chronic swelling and abnormal myelination during secondary degeneration after partial injury to a central nervous system tract. J Neurotrauma. June 2011. 28(6): 1077-88
    http://www.ncbi.nlm.nih.gov/pubmed/21381867

  8. Fitzgerald M, Payne SC, Bartlett CA, Evill L, Harvey AR, Dunlop SA. Secondary retinal ganglion cell death and the neuroprotective effects of the calcium channel blocker lomerizine. November 2009. Invest Opthalmol Vis Sci. 50:5456-5462
    http://www.ncbi.nlm.nih.gov/pubmed/19474405

  9. Fitzgerald M, Bartlett C.A, Payne S.C, Hart N.S, Rodger J, Harvey A.R, Dunlop S.A. Near infrared light reduces oxidative stress and preserves function in CNS tissue vulnerable to secondary degeneration following partial transection of the optic nerve. November 2010. J Neurotrauma. 27(11): 2107-2119
    http://www.ncbi.nlm.nih.gov/pubmed/20822460



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