TLR4 and Alzheimer disease: Indeed, we found an increase of the proinflammatory mediator p-NF-κB in the cortical gray matter of the WE case compared with control, as well as in the positive-AD-control, with a predominant expression or nuclear localization, indicating that this proinflammatory factor is active, which is, presumably, a direct consequence of the activation of the TLR4 signaling in the frontal cortex.