Myelin repair after traumatic brain injury in early life
- Research Opportunity
- Project Status
- Medicine and Radiology
- Royal Melbourne Hospital
|Dr Bridgette Sempleemail@example.com||+61 3 90356379||Personal web page|
Damage to myelin, the insulating sheath surrounding nerves, is a common consequence of traumatic brain injury. Emerging evidence suggests that white matter connectivity problems may underlie social behaviour deficits in other contexts (e.g. autism spectrum disorders), and that enhancing myelination during this critical period of development may reverse these deficits, suggesting that myelination may be a key neuropathological mechanism underlying poor outcomes after brain injury during early life.
Previous findings by our group have found that the neurotrophin, brain-derived neurotrophic factor, enhances myelination by signalling through the TrkB receptor expressed on myelin-producing oligodendrocytes. Here, we aim to: (a) examine the consequences of brain injury in early life on postnatal myelin development, and (b) test whether a specific TrkB agonist can preserve and repair myelin following traumatic brain injury. Experiments may involve behavioural assays, animal handling, and immunohistochemical analysis to evaluate oligodendrocytes, cell death, myelin integrity and TrkB activation. Our findings will provide new proof-of-concept evidence that myelin integrity is critical to functional and neuropathological outcomes, and pave the way for future therapeutic applications.
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