IL1B and Alzheimer disease: Previous studies have shown a correlation between p38 MAPK activation and a decline in synaptophysin levels in AD transgenic mouse models and in primary microglia and cortical neuron co-cultures stimulated with LPS [48,49], and pharmacological inhibition of p38α MAPK significantly reduced TNFα and IL-1β production and prevented synaptophysin loss in an AD mouse model [24].