Effect of beta-amyloid peptides on alpha-7 nicotinic receptor status in astrocytes and neurons, and its relationship to pathogenesis of Alzheimer's disease / 中华病理学杂志
Chinese Journal of Pathology
;
(12): 462-466, 2006.
Article
in Chinese
| WPRIM
| ID: wpr-268932
ABSTRACT
<p><b>OBJECTIVE</b>To study the alterations of alpha-7 nicotinic receptor (nAChR) status in human brain tissues with Alzheimer's disease (AD) and mouse brain tissues with Swedish APP670/671 gene mutation, and to study the effect of beta-amyloid peptides (A-beta) on alpha-7 nAChR status in cultured astrocytes and neurons.</p><p><b>METHODS</b>Postmortem brain tissues from patients with AD and mouse brain tissues with Swedish APP mutation were collected. The expression of alpha-7 nAChR on astrocytes and neurons was detected by immunohistochemistry (ABC method). The alpha-7 nAChR protein level was measured by Western blotting. On the other hand, cultured astrocytes and neurons were treated with different concentrations of A-beta 25 - 35. The alpha-7 nAChR protein level was then measured.</p><p><b>RESULTS</b>Increased number of astrocytes surrounding senile plaques was observed in AD brain tissues. In AD brain tissues, as compared to age-matched controls, alpha-7 nAChR protein level was increased in astrocytes, but decreased in neurons. High level of alpha-7 nAChR protein was also observed in mouse brain tissues with APP mutation. Exposure to A-beta 25 - 35 induced an increase (up to 38%) in alpha-7 nAChR protein level in astrocytes but a decrease (up to 32%) in neurons.</p><p><b>CONCLUSIONS</b>Decrease in alpha-7 nAChR level in neurons may be related to the pathogenesis of AD, whereas an increased level of alpha-7 nAChR in astrocytes, as induced by excessive A-beta, may represent a compensatory neuroprotective response.</p>
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Pathology
/
Peptide Fragments
/
Pharmacology
/
Brain
/
Immunohistochemistry
/
Immunoblotting
/
Cells, Cultured
/
Chemistry
/
Astrocytes
/
Amyloid beta-Peptides
Type of study:
Etiology study
Limits:
Aged80
/
Animals
/
Humans
/
Male
Language:
Chinese
Journal:
Chinese Journal of Pathology
Year:
2006
Type:
Article
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