Although chronic 17b-estradiol (E 2 ) has been shown to be a cognition-preserving and neuroprotec... more Although chronic 17b-estradiol (E 2 ) 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 E 2 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-b). The current study tests the hypothesis that long-term periodic E 2 -treatment improves cognition and reduces post-ischemic hippocampal injury by means of ER-b activation. Ovariectomized rats were given ten injections of E 2 at 48 hr intervals for 21 days. Hippocampal-dependent learning, memory and ischemic neuronal loss were monitored. Results demonstrated that periodic E 2 treatments improved spatial learning, memory and ischemic neuronal survival in ovariectomized rats. Additionally, periodic ER-b agonist treatments every 48 hr improved post-ischemic cognition. Silencing of hippocampal ER-b attenuated E 2 -mediated ischemic protection suggesting that ER-b plays a key role in mediating the beneficial effects of periodic E 2 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. Citation: Raval AP, Borges-Garcia R, Javier Moreno W, Perez-Pinzon MA, Bramlett H (2013) Periodic 17b-Estradiol Pretreatment Protects Rat Brain from Cerebral Ischemic Damage via Estrogen Receptor-b. PLoS ONE 8(4): e60716.
Although chronic 17b-estradiol (E 2 ) has been shown to be a cognition-preserving and neuroprotec... more Although chronic 17b-estradiol (E 2 ) 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 E 2 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-b). The current study tests the hypothesis that long-term periodic E 2 -treatment improves cognition and reduces post-ischemic hippocampal injury by means of ER-b activation. Ovariectomized rats were given ten injections of E 2 at 48 hr intervals for 21 days. Hippocampal-dependent learning, memory and ischemic neuronal loss were monitored. Results demonstrated that periodic E 2 treatments improved spatial learning, memory and ischemic neuronal survival in ovariectomized rats. Additionally, periodic ER-b agonist treatments every 48 hr improved post-ischemic cognition. Silencing of hippocampal ER-b attenuated E 2 -mediated ischemic protection suggesting that ER-b plays a key role in mediating the beneficial effects of periodic E 2 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. Citation: Raval AP, Borges-Garcia R, Javier Moreno W, Perez-Pinzon MA, Bramlett H (2013) Periodic 17b-Estradiol Pretreatment Protects Rat Brain from Cerebral Ischemic Damage via Estrogen Receptor-b. PLoS ONE 8(4): e60716.
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Papers by William Moreno