Numerous markers of inflammation have been reported in the Alzheimer's disease brain. Although other pathogenic mechanisms certainly apply, there is now compelling evidence that inflammation is not simply a response to already existing Alzheimer's pathology, but ultimately becomes a significant source of pathology. The pathogenic potential of inflammation in Alzheimer's disease follows from the inherent destructiveness of inflammatory mechanisms, the postmitotic status of neurons, and the unique interactions of inflammatory markers and cells with pathologic hallmarks of Alzheimer's such as amyloid beta-peptide. These conclusions from basic science are borne out by recent clinical efforts, though the latter are still limited and require further confirmation.