Recent studies suggest that inflammatory activation occurs in the brains of patients with Alzheimer's disease (AD). Several transcription factors such as nuclear factor-kappaB (NF-kappaB) and signal transducer and activator of transcription-1 (STAT1) may be activated in glial cells by a number of cytokines and then translocated from the cytosol to the nucleus. We assessed NF-kappaB and STAT1 in temporal cortex from normal and AD brains using specific antibodies. NF-kappaB p65 in the particulate fraction and STAT1alpha in both the particulate and cytosolic fractions were more abundant in AD cases than in controls. These findings suggest that the increased NF-kappaB and STAT1alpha in cell nuclei may be involved in inflammatory activation in AD brains.