A novel simple traumatic brain injury mouse model

Abstract

Background Traumatic brain injury, one of the leading causes of death in adults under 40 years of age in the world, is frequently caused by mechanical shock, resulting in diffuse neuronal damage and long-term cognitive dysfunction. Many existing TBI animal models revival with expensive equipment or special room are needed or the processes of operations are complex and not easy to be widely used. Therefore, a simpler TBI model needs to be designed. Methods Our TBI model is an innovation of the modeling method through air guns shutting rubber bullets. A core facet is the application of our designed rubber bullet impact device. It could focus the hitting power to the fixed site of the brain, thus triggering a mild closed head injury. Moreover, the degree of damage can be adjusted by the times of shots. Results Our model induced blood-brain barrier leakage and diffused neuronal damage. Besides, it led to an increased level of Tau phosphorylation and resulted in cognitive dysfunction within several weeks post-injury. Conclusion Our TBI model is not only simple and time-saving but also can simulate mild brain injuries in clinical. It is suitable for exploring pathobiological mechanisms as well as a screening of potential therapies for TBI.

Molecular Mechanisms Underlying Neuroinflammation Elicited by Occupational Injuries and Toxicants

“…TBI is characterized as one of the leading causes of death and disabling occupational injuries [136][137][138], with a high incidence rate in both the military and civilian populations [139]. Nearly 5.3 million people live with TBI in the U.S. [136,137,[140][141][142], including work-related TBI.…”

“…Immune cell activation and inflammatory responses are the cardinal features of traumatic injury. However, poor or failed resolution of acute inflammation, and compromise of the defense mechanisms, can contribute to chronic inflammation or an exaggerated systemic inflammatory response syndrome (SIRS) [138]. SIRS occurs shortly after trauma or traumatic injury when inflammatory cytokines enlist peripheral leukocytes to the site of the inflamed or injured tissue [138,146].…”