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Periodic 17beta-estradiol pretreatment protects rat brain from cerebral ischemic damage via estrogen receptor-beta.

Authors: Raval, AP  Borges-Garcia, R  Javier Moreno, W  Perez-Pinzon, MA  Bramlett, H 
Citation: Raval AP, etal., PLoS One. 2013 Apr 12;8(4):e60716. doi: 10.1371/journal.pone.0060716. Print 2013.
Pubmed: (View Article at PubMed) PMID:23593292
DOI: Full-text: DOI:10.1371/journal.pone.0060716

Although chronic 17beta-estradiol (E2) has been shown to be a cognition-preserving and neuroprotective agent in animal brain injury models, concern regarding its safety was raised by the failed translation of this phenomenon to the clinic. Previously, we demonstrated that a single bolus of E2 48 hr prior to ischemia protected the hippocampus from damage in ovariectomized rats via phosphorylation of cyclic-AMP response element binding protein, which requires activation of estrogen receptor subtype beta (ER-beta). The current study tests the hypothesis that long-term periodic E2-treatment improves cognition and reduces post-ischemic hippocampal injury by means of ER-beta activation. Ovariectomized rats were given ten injections of E2 at 48 hr intervals for 21 days. Hippocampal-dependent learning, memory and ischemic neuronal loss were monitored. Results demonstrated that periodic E2 treatments improved spatial learning, memory and ischemic neuronal survival in ovariectomized rats. Additionally, periodic ER-beta agonist treatments every 48 hr improved post-ischemic cognition. Silencing of hippocampal ER-beta attenuated E2-mediated ischemic protection suggesting that ER-beta plays a key role in mediating the beneficial effects of periodic E2 treatments. This study emphasizes the need to investigate a periodic estrogen replacement regimen to reduce cognitive decline and cerebral ischemia incidents/impact in post-menopausal women.

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RGD Object Information
RGD ID: 7364962
Created: 2013-10-14
Species: All species
Last Modified: 2013-10-14
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.