1.Changes in expression of synaptic proteins in brains of patients with Alzheimer's disease.
Ying CAO ; Rivka RAVID ; Zhi-zhong GUAN
Chinese Journal of Pathology 2009;38(12):833-834
Aged
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Aged, 80 and over
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Alzheimer Disease
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metabolism
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pathology
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Brain
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metabolism
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Dentate Gyrus
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metabolism
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Dynamin I
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metabolism
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Hippocampus
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metabolism
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Humans
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Monomeric Clathrin Assembly Proteins
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metabolism
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Neuropil
;
metabolism
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Synaptophysin
;
metabolism
2.Changes of nuclear factor and inflammatory chemotactic factors in brain of patients with Alzheimer's disease.
Yuan LIAO ; Zhi-zhong GUAN ; Rivka RAVID
Chinese Journal of Pathology 2011;40(9):585-589
OBJECTIVESTo 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.
METHODSTen 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.
RESULTSAs 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.
CONCLUSIONCorrelative 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.
Aged ; Aged, 80 and over ; Alzheimer Disease ; metabolism ; pathology ; Brain ; metabolism ; pathology ; Chemokine CCL2 ; metabolism ; Chemokine CCL3 ; metabolism ; Female ; Frontal Lobe ; metabolism ; pathology ; Glial Fibrillary Acidic Protein ; metabolism ; Hippocampus ; metabolism ; pathology ; Humans ; Immunohistochemistry ; Male ; Neuroglia ; metabolism ; pathology ; Plaque, Amyloid ; metabolism ; pathology ; Temporal Lobe ; metabolism ; pathology ; Transcription Factor RelA ; metabolism