Journal
JOURNAL OF NEUROENDOCRINOLOGY
Volume 24, Issue 1, Pages 34-47Publisher
WILEY
DOI: 10.1111/j.1365-2826.2011.02185.x
Keywords
stroke; hippocampus; cerebral cortex; menopause; ovariectomy
Categories
Funding
- NINDS [NS050730]
- National Institutes of Health, United States of America
- American Heart Association
Ask authors/readers for more resources
17 beta-Oestradiol (E2) is an important hormone signal that regulates multiple tissues and functions in the body. This review focuses on the neuroprotective actions of E2 in the brain against cerebral ischaemia and the potential underlying mechanisms. A particular focus of the review will be on the role of E2 to attenuate NADPH oxidase activation, superoxide and reactive oxygen species generation and reduce oxidative stress in the ischaemic brain as a potentially key neuroprotective mechanism. Evidence of a potential novel role of extranuclear oestrogen receptors in mediating E2 signalling and neuroprotective actions is also discussed. An additional subject is the growing evidence indicating that periods of long-term oestrogen deprivation, such as those occurring after menopause or surgical menopause, may lead to loss or attenuation of E2 signalling and neuroprotective actions in the brain, as well as enhanced sensitivity of the hippocampus to ischaemic stress damage. These findings have important implications with respect to the critical period hypothesis, which proposes that oestrogen replacement must be initiated at peri-menopause in humans to exert its beneficial cardiovascular and neural effects. The insights gained from these various studies will prove valuable for guiding future directions in the field.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available