Interestingly, and somewhat surprisingly, several groups, using both immunohistochemistry and ELISA as measurements, have observed that injection of inflammatory cytokines can also result in decreased Aβ. Work from our laboratory, in which the APP/PS1 Alzheimer’s disease mouse [142] was crossed with a mouse that conditionally expressed IL-1β, demonstrated that four weeks of sustained inflammation led to decreased Aβ plaque deposition as opposed to enhanced pathology [143]. Other groups have observed similar effects with different proinflammatory mediators and cytokines, such as lipopolysaccharide, IFNγ, TNFα, and IL-6 [144-147]. At first, this does not seem consistent with the in-vitro observations of inflammatory cytokines impairing Aβ clearance; however, one important distinction is that the in-vitro experiments exist in a closed system. Single treatments with cytokines in vitro impair phagocytic functions of microglia but do not take into account other cells and how they react to the inflammatory state in vivo. As previously mentioned, there is an established pattern of immune cell activation during inflammation. Initially there is a proinflammatory response, which gives way to an anti-inflammatory response that mitigates and repairs damage. Cells capable
