Estrogen neuroprotection and the critical period hypothesis.

Estrogen neuroprotection and the critical period hypothesis.
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DOI:
10.1016/j.yfrne.2011.10.001
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发表时间:
2012-01
影响因子:
7.4
通讯作者:
Brann, Darrell
Brann, Darrell
中科院分区:
医学1区
文献类型:
--
作者:
Scott, Erin;Zhang, Quan-guang;Wang, Ruimin;Vadlamudi, Ratna;Brann, Darrell

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17β-雌二醇(E2)是一种神经退行性疾病。本文综述了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,雌二醇在大脑中的有益作用存在一个“关键时期”。潜在的机制的关键时期进行了讨论,是神经系统的后果,长期E2剥夺(LTED)在动物和人类自然绝经或手术绝经后。我们还总结了有关绝经后激素治疗(HT)的主要临床试验,比较其结果与心血管和神经系统疾病,并讨论其相关性的关键期假说。最后,潜在的警告,争议和该领域的未来发展方向,强调和讨论整个审查。
17β-estradiol (estradiol or E2) is implicated as a 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.
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发表时间: 2008-08-01
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