Figure 7

Working model. Peripheral injury leads to a systemic inflammatory response and release of danger-associated molecular patterns (DAMPs) in the circulation causing neuroinflammation and subsequent cognitive decline. Postoperative infection elicits a secondary hit that exacerbates the proinflammatory milieu and CNS dysfunction. Stimulation of the cholinergic antiinflammatory signaling pathway via selective α7 nAChR improves cognitive decline though modulation of NF-κB and oxidative stress activity on monocytes, thus attenuating neuroinflammation and dampening the systemic proinflammatory milieu.