Much evidence has accumulated to suggest that the peripheral type benzodiazepine (PBZ) binding site has a predominantly glial localization. Elevated PBZ binding densities have been reported in various models of brain damage, apparently reflecting glial proliferation in response to neurodegeneration. In the present study, PBZ receptor densities were examined in frontal and temporal cortex of Alzheimer's disease (AD) patients using the ligand [3H]PK 11195. There was a highly significant (p less than 0.01) increase in PBZ binding sites in the temporal cortex from AD patients. In the frontal cortex, a moderate increase was observed that approached statistical significance (p = 0.07). Decreased choline acetyltransferase activity was observed in both regions. These findings offer support for the potential use of the PBZ binding site as a marker for gliosis associated with neuronal cell death.