TBI, Neurodegenerative Disease, and Proteinopathies

Project Details

Traumatic brain injury (TBI) is a neurodegenerative disease that is induced by forces applied to the brain, and it is also a known risk factor for a number of other neurodegenerative conditions. There is currently no drug that is known to improve long-term outcomes in TBI survivors. TBI has been shown to induce proteinopathies in the brain involving tau, amyloid beta, and or TDP-43, and each of the proteins has been implicated in neurodegenertative conditions that TBI is associated with (e.g., Alzheimer's, ALS).

This project makes use of rodent models of TBI to characterize proteinopathies post-injury and develop novel pharmaceutical interventions to target these abnormalities and mitigate neurodegeneration. We also use post-mortem human TBI tissue to validate that the same changes occur in human TBI patients. Ulimately our goal is to develop therapies that can be used in the clinical setting.

Researchers

  • Shijie Liu, Postdoctoral Fellow
  • David Wright, NIF Fellow, PhD Student
  • Lily Taylor, Research Assistant
  • Xin Tan, PhD Student
  • Ping Zheng, PhD Student
  • Stefanie Bird, Masters Student

Collaborators

  • Dr. Bradley Turner, Florey Neuroscience Institute, The University of Melbourne
  • Professors Terence O’Brien, Chris Hovens, and Nigel Jones, The University of Melbourne

Funding

  • Australian National Health and Medical Research Council (NHMRC)
  • The Motor Neurone Disease Research Institute of Australia (MNDRIA)

Research Opportunities

This research project is available to PhD students to join as part of their thesis.
Please contact the Research Group Leader to discuss your options.

Research Outcomes

  1. Tan XL, Wright DK, Liu S, Hovens C, O'Brien TJ, Shultz SR. Sodium selenate, a
    protein phosphatase 2A activator, mitigates hyperphosphorylated tau and improves
    repeated mild traumatic brain injury outcomes. Neuropharmacology. 2016 May
    7;108:382-393. doi: 10.1016/j.neuropharm.2016.05.001. [Epub ahead of print]
    PubMed PMID: 27163189.
  2. Shultz SR, Wright DK, Zheng P, Stuchbery R, Liu SJ, Sashindranath M, Medcalf
    RL, Johnston LA, Hovens CM, Jones NC, O'Brien TJ. Sodium selenate reduces
    hyperphosphorylated tau and improves outcomes after traumatic brain injury.
    Brain. 2015 May;138(Pt 5):1297-313. doi: 10.1093/brain/awv053. Epub 2015 Mar 13.
    PubMed PMID: 25771151.
  3. Zheng P, Shultz SR, Hovens CM, Velakoulis D, Jones NC, O'Brien TJ.
    Hyperphosphorylated tau is implicated in acquired epilepsy and neuropsychiatric
    comorbidities. Mol Neurobiol. 2014 Jun;49(3):1532-9. doi:10.1007/s12035-013-8601-9. Epub 2013 Dec 10. Review. PubMed PMID: 24323428.

Research Publications

  1. Tan XL, Wright DK, Liu S, Hovens C, O'Brien TJ, Shultz SR. Sodium selenate, a
    protein phosphatase 2A activator, mitigates hyperphosphorylated tau and improves
    repeated mild traumatic brain injury outcomes. Neuropharmacology. 2016 May
    7;108:382-393. doi: 10.1016/j.neuropharm.2016.05.001. [Epub ahead of print]
    PubMed PMID: 27163189.
  2. Shultz SR, Wright DK, Zheng P, Stuchbery R, Liu SJ, Sashindranath M, Medcalf
    RL, Johnston LA, Hovens CM, Jones NC, O'Brien TJ. Sodium selenate reduces
    hyperphosphorylated tau and improves outcomes after traumatic brain injury.
    Brain. 2015 May;138(Pt 5):1297-313. doi: 10.1093/brain/awv053. Epub 2015 Mar 13.
    PubMed PMID: 25771151.
  3. Zheng P, Shultz SR, Hovens CM, Velakoulis D, Jones NC, O'Brien TJ.
    Hyperphosphorylated tau is implicated in acquired epilepsy and neuropsychiatric
    comorbidities. Mol Neurobiol. 2014 Jun;49(3):1532-9. doi:10.1007/s12035-013-8601-9. Epub 2013 Dec 10. Review. PubMed PMID: 24323428.

Research Group

Translational Traumatic Brain Injury Laboratory



Faculty Research Themes

Neuroscience

School Research Themes

Neuroscience & Psychiatry



Key Contact

For further information about this research, please contact the research group leader.

Department / Centre

Medicine and Radiology