Profiling the neuroimmune cascade in 3xTg mice exposed to successive mild traumatic brain injuries
Repetitive mild traumatic brain injuries (rmTBI) sustained within a window of vulnerability can result in long term cognitive deficits, depression, and eventual neurodegeneration associated with tau pathology, amyloid beta plaques, gliosis, and neuronal and functional loss. However, we have limited understanding of how successive injuries affect the brain to result in these devastating long-term consequences. In the current study, we addressed the question of how repeated injuries affect the brain in the acute phase of injury (<24hr) by exposing the 3xTg-AD mouse model of tau and amyloid beta pathology to successive (1x, 3x, 5x) once-daily weight drop closed-head injuries and quantifying transcription at 30min, 4hr, and 24hr after each injury. Overall design: Left somatomotor cortices of female triple transgenic (3xTg-AD) mice exposed to successive weight drop closed-head injuries. Three injury groups (1x, 3x, 5x) across four time points (pre-injury and 30m, 4h, & 24h post-injury) (n=3-4 per group, 40 total). Sample 30 was removed during analysis due to outlier status from corresponding protein data.