Institute of Molecular Medicine and Genetics, Georgia Health Sciences University, Augusta, GA 30912, USA.
Front Neuroendocrinol. 2012 Jan;33(1):85-104. doi: 10.1016/j.yfrne.2011.10.001. Epub 2011 Nov 4.
17β-Estradiol (estradiol or E2) is implicated as a neuroprotective factor in a variety of neurodegenerative disorders. This review focuses on the mechanisms underlying E2 neuroprotection in cerebral ischemia, as well as emerging evidence from basic science and clinical studies, which suggests that there is a "critical period" for estradiol's beneficial effect in the brain. Potential mechanisms underlying the critical period are discussed, as are the neurological consequences of long-term E2 deprivation (LTED) in animals and in humans after natural menopause or surgical menopause. We also summarize the major clinical trials concerning postmenopausal hormone therapy (HT), comparing their outcomes with respect to cardiovascular and neurological disease and discussing their relevance to the critical period hypothesis. Finally, potential caveats, controversies and future directions for the field are highlighted and discussed throughout the review.
17β-雌二醇（雌二醇或 E2）被认为是多种神经退行性疾病的神经保护因子。这篇综述重点介绍了 E2 在脑缺血中的神经保护机制，以及基础科学和临床研究中的新证据，这些证据表明，在大脑中存在一个“关键时期”，E2 的有益作用。讨论了关键时期潜在的机制，以及动物中长期剥夺雌二醇（LTED）以及自然绝经或手术绝经后人类的神经学后果。我们还总结了有关绝经后激素治疗（HT）的主要临床试验，比较了它们在心血管和神经疾病方面的结果，并讨论了它们与关键时期假说的相关性。最后，在整个综述中强调并讨论了该领域的潜在注意事项、争议和未来方向。
