NF-kB immunoreactivity is observed in association with beta A4 diffuse plaques in patients with Alzheimer's disease.

Transcription factor NF-kB is widely expressed in the nervous system and, particularly, in synaptic terminals. Increased NF-kB expression in synaptosomes has been observed as a result of activity, and beta A4 deposition. In the present study we have examined NF-kB immunoreactivity, by means of NF-kB p65 immunohistochemistry, in the brains of seven patients with Alzheimer's disease, two patients with Creutzfeldt-Jakob disease associated with PrP amyloid deposition, and seven age-matched controls. Our purpose was to examine possible NF-kB induction associated to beta A4 or PrP deposition in these diseases. Punctate NF-kB immunoreactivity was constantly found in the neuropil of diffuse beta A4 deposits but not in dystrophic neurites of senile plaques. In addition, NF-kB immunoreactivity was found in the nuclei of neurons, but not in the nuclei of reactive astrocytes, in the vicinity of diffuse plaques, thus suggesting NF-kB translocation to the nucleus. Finally, a few neurons with neurofibrillary degeneration showed increased cytoplasmic NF-kB immunoreactivity probably secondary to abnormal compartmentation or impaired transport of NF-kB. No similar modifications in NF-kB immunoreactivity were observed in association with PrP deposits in patients with Creutzfeldt-Jakob disease. Since it has been suggested that the presence of NF-kB in synapses may indicate the existence of a new pathway of gene transcription, the present results support the concept that this pathway may be activated by the deposition of beta A4 in diffuse plaques in Alzheimer's disease.