Journal
FRONTIERS IN NEUROENDOCRINOLOGY
Volume 32, Issue 3, Pages 336-352Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.yfrne.2010.12.005
Keywords
Stroke; Global ischemia; Neuroprotection; Estradiol; Hippocampus; Estrogen receptor; Insulin-like growth factor-1; GPR30; Apoptosis; CREB
Categories
Funding
- American Heart Association [R01 MH41414, R01 NS045693, R01 AG AG027702, 0335285N]
- ISCIII RETICS-RENEVAS [RD06/0026/0006]
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This review highlights our investigations into the neuroprotective efficacy of estradiol and other estrogenic agents in a clinically relevant animal model of transient global ischemia, which causes selective, delayed death of hippocampal CA1 neurons and associated cognitive deficits. We find that estradiol rescues a significant number of CA1 pyramidal neurons that would otherwise die in response to global ischemia, and this is true when hormone is provided as a long-term pretreatment at physiological doses or as an acute treatment at the time of reperfusion. In addition to enhancing neuronal survival, both forms of estradiol treatment induce measurable cognitive benefit in young animals. Moreover, estradiol and estrogen analogs that do not bind classical nuclear estrogen receptors retain their neuroprotective efficacy in middle-aged females deprived of ovarian hormones for a prolonged duration (8 weeks). Thus, non-feminizing estrogens may represent a new therapeutic approach for treating the neuronal damage associated with global ischemia. (C) 2010 Elsevier Inc. All rights reserved.
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