AI Article Synopsis
- The study aimed to explore whether dexamethasone (DEX) worsens learning and memory problems caused by amyloid beta-protein (Abeta) in rats, focusing on its effects on the hippocampus.
- Using tools like the Morris water maze, researchers found that DEX indeed amplified Abeta-induced cognitive impairments and caused noticeable changes in the hippocampal CA1 region, including elevated levels of phosphorylated tau protein.
- The findings suggest that DEX might contribute to cognitive decline related to Alzheimer's disease by increasing phosphorylated tau and p25 protein levels, especially since both Abeta and glucocorticoids tend to rise with age.
Article Abstract
Objective: To determine whether dexamethasone (DEX) could potentiate amyloid beta-protein (Abeta)-induced learning and memory impairment in rats, and, if so, what the underlying mechanism is.
Methods: Morris water maze was used to investigate whether DEX could potentiate Abeta-induced learning and memory impairment in rats, and the histopathologic changes in CA1 field of hippocampus were examined under a light microscope. Immunohistochemistry was used to observe the change of the phosphorylated tau at Thr-231 in the CA1 field of hippocampus. The effects of DEX on the levels of phospho-tau and p25 induced by Abeta were analyzed by Western blot.
Results: The results showed that DEX could potentiate Abeta-induced learning and memory impairment and pathological damage in CA1 field of hippocampus in Sprague Dawley (SD) rats, and could enhance the increased levels of phosphorylated tau induced by Abeta(25-35) in the neuronal cell bodies in CA1 field of hippocampus of SD rats and in the protein extracts from hippocampus. Pretreatment of hippocampal neurons with DEX could up-regulate the increased levels of phosphorylated tau and p25 protein induced by Abeta(25-35) in vitro.
Conclusions: These results suggest that DEX could potentiate Abeta-induced learning and memory impairment and pathological damage in CA1 field of hippocampus in SD rats, which might be related to DEX up-regulating the levels of phosphorylated tau and p25 protein induced by Abeta(25-35). Since Abeta and glucocorticoids increase with aging, DEX potentiating Abeta-induced learning and memory impairment may be one of the etiology of Alzheimer's disease.
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| http://dx.doi.org/10.1179/016164110X12816242542698 | DOI Listing |
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