Mitochondrial dysfunction and neuroinflammation occur in Alzheimer’s disease (AD). The
causes of these pathologic lesions remain uncertain, but links between these phenomena are increasingly
recognized. In this review, we discuss data that indicate mitochondria or mitochondrial components
may contribute to neuroinflammation. While mitochondrial dysfunction could cause neuroinflammation,
neuroinflammation could also cause mitochondrial dysfunction. However, based on the systemic nature of
AD mitochondrial dysfunction as well as data from experiments we discuss, the former possibility is perhaps more likely.
If correct, then manipulation of mitochondria, either directly or through manipulations of bioenergetic pathways, could
prove effective in reducing metabolic dysfunction and neuroinflammation in AD patients. We also review some potential
approaches through which such manipulations may be achieved.