Because we aimed to identify relationships between immune signaling and molecular markers associated with AD-related pathology, and wild-type mice show inconsistent evidence of pathological changes after TBI [52–54], we used the triple transgenic model of Alzheimer’s-like pathology (3xTg-AD), which contains human mutant forms of genes in the Aβ processing pathway (APP, PSEN1) and tau (MAPT). The gene discussed is PSEN1; the disease is Alzheimer disease.