title: Dexamethasone potentiated Aβ-induced learning and memory impairment in rats.
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.
authors.affiliation: Department of Laboratory Medcine, Anhui Medical University, Hefei, China.
authors.forename: Yu-You
authors.initials: YY
authors.lastname: Yao
authors.forename: Qing-Si
authors.initials: QS
authors.lastname: Wu
authors.forename: Wei-Zu
authors.initials: WZ
authors.lastname: Li
authors.forename: Wei-Ping
authors.initials: WP
authors.lastname: Li
mesh_terms: D000544:Alzheimer Disease / Q000188:drug therapy* / Q000378:metabolism / Q000523:psychology; D016229:Amyloid beta-Peptides / Q000378:metabolism / Q000633:toxicity*; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000009:adverse effects*; D002478:Cells, Cultured; D003907:Dexamethasone / Q000009:adverse effects*; D004195:Disease Models, Animal; D004357:Drug Synergism; D005260:Female; D007859:Learning Disabilities / Q000139:chemically induced* / Q000523:psychology; D008297:Male; D008569:Memory Disorders / Q000139:chemically induced* / Q000523:psychology; D009474:Neurons / Q000187:drug effects* / Q000473:pathology; D010446:Peptide Fragments / Q000378:metabolism / Q000633:toxicity*; D011247:Pregnancy; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D016229:Amyloid beta-Peptides; D000893:Anti-Inflammatory Agents; D010446:Peptide Fragments; C074636:amyloid beta-protein (25-35); D003907:Dexamethasone