Therefore, in this study, the effect of TBI on the exacerbation of Alzheimer's-like cognitive dysfunction and pathology in amyloid-β precursor protein (APP)/presenilin 1 (PS1) transgenic mice, as well as the potential mechanism related to the activation and phenotype of microglia following TBI, was assessed in an attempt to provide preclinical evidence supporting TBI-triggered AD progression. The gene discussed is APP; the disease is Alzheimer disease.