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NF‐kB immunoreactivity is observed in association with βA4 diffuse plaques in patients with Alzheimer’s disease
Author(s) -
Isidró Ferrer,
Eulàlia Martı́,
Elena López,
Avelina Tortosa
Publication year - 1998
Publication title -
neuropathology and applied neurobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.538
H-Index - 95
eISSN - 1365-2990
pISSN - 0305-1846
DOI - 10.1046/j.1365-2990.1998.00116.x
Subject(s) - senile plaques , pathology , neuropil , immunohistochemistry , neurofilament , degenerative disease , nf κb , pathogenesis , neurite , biology , alzheimer's disease , p50 , nucleus , transcription factor , central nervous system , disease , medicine , microbiology and biotechnology , gene , endocrinology , signal transduction , genetics , in vitro
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 βA4 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 βA4 or PrP deposition in these diseases. Punctate NF‐kB immunoreactivity was constantly found in the neuropil of diffuse βA4 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 βA4 in diffuse plaques in Alzheimer’s disease.