Abstract
Traumatic brain injury (TBI) causes substantial mortality and disability, but effective treatments are unavailable. An external force causes primary injury, which is followed by secondary injury that triggers chronic neurodegenerative diseases. Therefore, understanding the mechanisms underlying post-TBI secondary injury might provide insights into neurodegenerative diseases. The secondary injury is known to share some physiological features with neurodegenerative diseases. So far, many TBI models in mammals exist, but models in other species are required from the viewpoint of lifespan and animal welfare. In Drosophila, closed and open TBI models are available. Both models have focused on TBI-induced changes in innate immunity. Aging strongly induces innate immunity responses, and neuroinflammation plays an important role in both mammalian models of TBI and humans with TBI. Although Drosophila models do not mimic all phenomena involved in post-TBI secondary injury in mammals, further experiments with Drosophila models and other animal models could elucidate the mechanisms involved in post-TBI secondary brain injury, which would in turn elucidate neurodegenerative processes.
