title: [Changes of nuclear factor and inflammatory chemotactic factors in brain of patients with Alzheimer's disease].
abstract: OBJECTIVE
  To investigate the changes of nuclear factor (NF-)κBp65 and inflammatory chemotactic factors including monocyte chemoattractant protein 1 (MCP-1/CCL-2), macrophage inflammatory protein 1α (MIP-1α/CCL-3), glial fibrillary acidic protein (GFAP) in brains of the patients with Alzheimer's disease (AD) and reveal the correlation of these factors.
  
  
  METHODS
  Ten patients with AD and 8 age-matched control subjects were selected in the study. Immunohistochemistry was performed to determine the protein expression of NF-κBp65, MCP-1, MIP-1α and GFAP. Double-immunohistochemistry was used to detect the expression of GFAP and β-amyloid peptide 1-42 (Aβ(1-42)) in the hippocampus, temporal and frontal cortices.
  
  
  RESULTS
  As compared to age-matched controls (the numbers of the positively stained neuronal cells: 0.31 ± 0.20, 0.25 ± 0.20 and 0.25 ± 0.20, respectively), the immunoreactivities of NF-κBp65 in the hippocampus and the temporal and frontal cortices (numbers of the positively stained cells: 3.6 ± 1.5, 2.2 ± 1.2 and 2.2 ± 1.2, respectively) were significantly increased in AD brains. The levels of MCP-1 and MIP-1α in the hippocampus, and the temporal and frontal cortices (numbers of the positively stained neuronal cells: 8.0 ± 1.3, 8.8 ± 1.0, 9.3 ± 1.4, respectively;and 8.1 ± 1.5, 12.5 ± 1.1, 6.4 ± 1.1, respectively) with AD were significantly higher than those of controls (the numbers of the positive neuronal cells: 4.5 ± 0.9, 4.5 ± 0.6, 4.0 ± 1.8, respectively; and 5.0 ± 1.9, 6.3 ± 2.2, 3.8 ± 1.5, respectively). An increased number of glial cells stained with GFAP were observed to extensively distribute around the senile plaques in AD brains. There were significant correlations between NF-κBp65 and these inflammatory chemotactic factors in AD brains.
  
  
  CONCLUSIONS
  Correlative expressions of NF and inflammatory chemotactic factors were found in the brains of AD patients, through a mechanism that may involve the inflammatory response induced by Aβ in the processing of AD.
authors.affiliation: Department of Pathology, Guiyang Medical College, Guiyang 550004, China.
authors.forename: Yuan
authors.initials: Y
authors.lastname: Liao
authors.forename: Zhi-zhong
authors.initials: ZZ
authors.lastname: Guan
authors.forename: Rivka
authors.initials: R
authors.lastname: Ravid
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000544:Alzheimer Disease / Q000378:metabolism* / Q000473:pathology; D001921:Brain / Q000378:metabolism* / Q000473:pathology; D018932:Chemokine CCL2 / Q000378:metabolism*; D054405:Chemokine CCL3 / Q000378:metabolism*; D005260:Female; D005625:Frontal Lobe / Q000378:metabolism / Q000473:pathology; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism*; D006624:Hippocampus / Q000378:metabolism / Q000473:pathology; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D009457:Neuroglia / Q000378:metabolism / Q000473:pathology; D058225:Plaque, Amyloid / Q000378:metabolism / Q000473:pathology; D013702:Temporal Lobe / Q000378:metabolism / Q000473:pathology; D051996:Transcription Factor RelA / Q000378:metabolism*
chemical_list: C111835:CCL2 protein, human; D018932:Chemokine CCL2; D054405:Chemokine CCL3; D005904:Glial Fibrillary Acidic Protein; D051996:Transcription Factor RelA