IL1B and amyloidosis: Although our results are most consistent with the interpretation that increased microglia number is the mechanism underlying reduced Aβ plaque load in our model of sustained IL-1β overexpression, we have not addressed the possibility that microglia in this environment increase their uptake and degradation (e.g. flux) of fAβ or take up soluble forms of Aβ that contribute to overall amyloid plaque burden.