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Acta Physiologica Sinica ; (6): 142-146, 2003.
Article in Chinese | WPRIM | ID: wpr-318927

ABSTRACT

Recent evidence indicates that the aberrant neuronal expression of mitotic proteins in Alzheimer's disease (AD) brain may be related to AD pathological changes. To investigate whether the toxicity of beta-amyloid protein (Abeta) induces mitotic proteins expression in adult rat brain, we used immunohistochemical and integral optical density analytic method to analyze the adult rat brains, which had been injected with Abeta(25-35) into unilateral amygdala. Results showed that the levels of neurofibrillary tangle (NFT) related phosphorylated tau protein and apoptosis related protein Bax were increased in Abeta(25-35) injected rat brains, meanwhile the aberrantly expression of mitotic protein cyclin A and cyclin B1 was also detected at 7 d after operation, but the level of cyclin A decreased and cyclin B1 disappeared at 21 d. Immunofluorescence double labeling presented that cyclin B1 was partially co-localized with Bax or phosphorylated tau protein, whereas Bax and phosphorylated tau protein seldom co-localized. These results suggest that Abeta causes mitotic protein expression in adult brain neurons, which may die through apoptosis or may be affected by AD NFT-related tau phosphorylation.


Subject(s)
Animals , Male , Rats , Alzheimer Disease , Metabolism , Amygdala , Metabolism , Amyloid beta-Peptides , Toxicity , Cyclin A , Metabolism , Cyclin B1 , Metabolism , Neurons , Metabolism , Peptide Fragments , Toxicity , Phosphorylation , Random Allocation , Rats, Sprague-Dawley , bcl-2-Associated X Protein , Metabolism , tau Proteins , Metabolism
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