• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>BMC Neuroscience >Estrogen-Astrocyte interactions: Implications for neuroprotection
【24h】

Estrogen-Astrocyte interactions: Implications for neuroprotection

机译：雌激素与星形胶质细胞的相互作用：对神经保护的意义。

获取原文
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Background Recent work has suggested that the ovarian steroid 17β-estradiol, at physiological concentrations, may exert protective effects in neurodegenerative disorders such as Alzheimer's disease, Parkinson's disease and acute ischemic stroke. While physiological concentrations of estrogen have consistently been shown to be protective in vivo , direct protection upon purified neurons is controversial, with many investigators unable to show a direct protection in highly purified primary neuronal cultures. These findings suggest that while direct protection may occur in some instances, an alternative or parallel pathway for protection may exist which could involve another cell type in the brain. Presentation of the Hypothesis A hypothetical indirect protective mechanism is proposed whereby physiological levels of estrogen stimulate the release of astrocyte -derived neuroprotective factors, which aid in the protection of neurons from cell death. This hypothesis is attractive as it provides a potential mechanism for protection of estrogen receptor (ER)- negative neurons through an astrocyte intermediate. It is envisioned that the indirect pathway could act in concert with the direct pathway to achieve a more widespread global protection of both ER+ and ER- neurons. Testing the hypothesis We hypothesize that targeted deletion of estrogen receptors in astrocytes will significantly attenuate the neuroprotective effects of estrogen. Implications of the hypothesis If true, the hypothesis would significantly advance our understanding of endocrine-glia-neuron interactions. It may also help explain, at least in part, the reported beneficial effects of estrogen in neurodegenerative disorders. Finally, it also sets the stage for potential extension of the hypothetical mechanism to other important estrogen actions in the brain such as neurotropism, neurosecretion, and synaptic plasticity.
机译：背景技术最近的研究表明，以生理浓度的卵巢类固醇17β-雌二醇可能对神经退行性疾病（例如阿尔茨海默氏病，帕金森氏病和急性缺血性中风）发挥保护作用。尽管雌激素的生理浓度一直被证明在体内具有保护作用，但对纯化神经元的直接保护仍存在争议，许多研究者无法在高度纯化的原代神经元培养物中显示出直接保护作用。这些发现表明，尽管在某些情况下可能会发生直接保护，但可能存在另一种或平行的保护途径，可能涉及大脑中的另一种细胞类型。假设的提出提出了一种假设的间接保护机制，据此生理水平的雌激素刺激了星形胶质细胞源性神经保护因子的释放，从而有助于保护神经元免受细胞死亡。该假设很有吸引力，因为它提供了通过星形胶质细胞中间体保护雌激素受体（ER）阴性神经元的潜在机制。可以预见，间接途径可以与直接途径协同作用，以实现对ER +和ER-神经元的更广泛的全球保护。检验假设我们假设，星形胶质细胞中雌激素受体的靶向缺失会显着减弱雌激素的神经保护作用。假设的含义如果为真，则该假设将大大提高我们对内分泌-神经胶质-神经元相互作用的理解。它也可能至少部分有助于解释雌激素在神经退行性疾病中的有益作用。最后，它还为虚拟机制可能扩展到大脑中其他重要的雌激素作用（例如神经嗜性，神经分泌和突触可塑性）提供了条件。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号