Taken together, these results (summarized in Fig. 5) are consistent with the hypothesis that the exaggerated hippocampal inflammatory response produced by age and an infection might decrease availability of BDNF at hippocampal synapses, and thus contribute to deficits in forms of long-lasting memory and synaptic plasticity that require BDNF for their complete expression. The gene discussed is BDNF; the disease is infection.