2019 Semple group. L-R: Rishabh Sharma, Dr Akram Zamani, Erskine Chu, Dr Bridgette Semple, Laken Willis, Larissa Dill, Janet Leung
Neurotrauma, traumatic brain injury, inflammation, epilepsy, animal models, behaviour, paediatric
To understand the key biological mechanisms that contribute to poor long-term outcomes after traumatic brain injury, particularly during early childhood
Brain injuries in young children often results in debilitating and chronic consequences, including psychosocial and neurocognitive deficits which may persist or emerge as the brain matures. However, the biological mechanisms that underlie poor long-term outcomes following traumatic brain injury (TBI) to the young brain are poorly understood. Our overall research goal is therefore to better understand how the immature brain responds to injury, with a particular focus on the sub-acute and chronic periods after an injury. Ultimately, this knowledge will allow us to develop novel therapeutic interventions aimed at improving outcomes and quality of life for brain-injured patients.
Several ongoing research projects are centred around this theme, using a range of approaches including molecular and cellular methods, neuroimaging, in vivo electroencephalographic recordings, and behavioural assays. One of the most commonly reported consequences of paediatric TBI is a change in social behaviour; for example, a reduction in social interactions, increased social withdrawal and isolation, and associated psychiatric issues such as depression and anxiety. We have developed a model of paediatric TBI in which mice develop social behaviour deficits as they age to adults, consistent with the trajectory of social behaviour deficits frequently seen in brain-injured children. Using this model, we are now tackling fundamental unanswered questions about the underlying mechanisms of these behavioural changes after TBI, including the identification of risk and resilience factors, and the contribution of white matter degeneration. In addition, brain injuries are associated with a heightened risk of developing epilepsy, or recurrent seizure activity that may contribute to progressive neurodegeneration and infer with quality of life. Using a validated mouse model of TBI in the mouse, we are evaluating the contribution of key inflammatory cytokines and cellular mediators to seizure susceptibility and aberrant neuroplasticity.
Current Project Funding
- 2018-2020 Semple BD. NHMRC project grant 1122456. Social dysfunction after paediatric brain injury in mice.
- 2018-2021 Semple BD. NHMRC CDF level 1 1141347. Long-term outcomes after paediatric traumatic brain injury.
- 2017-18 Fletcher J and Semple BD. Project Funding from the Department of Anatomy and Neuroscience, The University of Melbourne. Myelin repair after early life brain injury.
See recent publications for Bridget Semple in the Monash RSS feed immediately below, at Pubmed and select list further down.
- Semple BD, O'Brien TJ, Gimlin K, Wright DK, Kim SE, Casillas-Espinosa PM, Webster KM, Petrou S, Noble-Haeusslein LJ. Interleukin-1 Receptor in Seizure Susceptibility after Traumatic Injury to the Pediatric Brain. J Neurosci. 2017 Aug 16;37(33):7864-7877. doi: 10.1523/JNEUROSCI.0982-17.2017. Epub 2017 Jul 19. PMID: 28724747
- Webster KM, Sun M, Crack P, O'Brien TJ, Shultz SR, Semple BD. Inflammation in epileptogenesis after traumatic brain injury. J Neuroinflammation. 2017 Jan 13;14(1):10. doi: 10.1186/s12974-016-0786-1. Review. PMID: 28086980
- Semple BD, Dixit S, Shultz SR, Boon WC, O'Brien TJ. Sex-dependent changes in neuronal morphology and psychosocial behaviors after pediatric brain injury. Behav Brain Res. 2017 Feb 15;319:48-62. doi: 10.1016/j.bbr.2016.10.045. Epub 2016 Nov 6. PMID: 27829127