Similar to the neurotoxicity effects of LRRK2 in experimental PD, our study showed that both the mRNA and protein levels of LRRK2 were increased in the injured brain region and peaked at 12 h after TBI, while inhibiting LRRK2 expression ameliorated TBI-induced neuronal apoptosis, brain edema, BBB permeability, and neurological impairment. Here, LRRK2 is linked to Parkinson disease.