Considering that the neuroprotective role of microglia develops early in the course of brain illness, the failure to detect elevated [11C]NE40 uptake in AD patients [23] is understandable, possibly because the microglia activated during the chronic state of neurodegeneration are considered to be acting as proinflammatory cells [24] or because the demise of neurons that also express CB2 reduces detectable radioactivity. Here, CNR2 is linked to Alzheimer disease.