How does Traumatic Brain Injury (TBI) affect the infant brain?
Brain development continues until late adolescence, meaning that a traumatic brain injury (TBI) perturbs different developmental milestones and cellular processes depending on age at injury. Juvenile TBI is doubly problematic: full recovery requires repair of damage, as in adults, but there is the additional burden of catching up with and then maintaining normal development. Production of oligodendrocytes and myelination is particularly susceptible to damage to the young brain, while production and maturation of new neurons and astrocytes is also disrupted. The effects of damage are likely to be different at pre-myelinating ages (infancy) compared to early childhood, when myelination production is high. We propose that, in addition to neuronal/axonal loss, perturbed oligodendrocyte and astrocyte development are major contributors to the enhanced deficits observed in juvenile TBI, leading to white matter tract and brain atrophy.
We have developed a novel model of infant TBI in mouse pups and our preliminary data shows perturbed oligodendrocyte development and behavioural deficits, thus our research is addressing the following broad aim:
Aim: To determine which cellular mechanisms contribute to neural deficits in mouse models of infant TBI (using 7 day old mice) by comparing the acute and chronic cellular and histological consequences of TBI and to correlate these with the altered physical, cognitive and social behaviours up to 4 months after TBI.