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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 Abeta25-35 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 Abeta25-35 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 Abeta25-35. 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.