Early studies reported that adjuvant therapy involving BDNF protects the brain from three distinct forms of injury in experimental bacterial meningitis [28]; however, here, we investigated the effects of BDNF/TrkB interaction on the inflammatory response and hippocampal apoptosis, as well as its effect on other potential intracellular signaling pathways responsible for this protective activity associated with PM. The gene discussed is BDNF; the disease is bacterial meningitis.