Neuroscience Research Center, Mashhad University of Medical Sciences, Mashhad, Iran.
Department of Neuroscience, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
Cell Mol Neurobiol. 2020 Apr;40(3):283-299. doi: 10.1007/s10571-019-00733-0. Epub 2019 Sep 9.
Alzheimer's disease (AD) is described as cognitive and memory impairments with a sex-related epidemiological profile, affecting two times more women than men. There is emerging evidence that alternations in the hippocampal neurogenesis occur at the early stage of AD. Therapies that may effectively slow, stop, or regenerate the dying neurons in AD are being extensively investigated in the last few decades, but none has yet been found to be effective. The regulation of endogenous neurogenesis is one of the main therapeutic targets for AD. Mounting evidence indicates that the neurosteroid estradiol (17β-estradiol) plays a supporting role in neurogenesis, neuronal activity, and synaptic plasticity of AD. This effect may provide preventive and/or therapeutic approaches for AD. In this article, we discuss the molecular mechanism of potential estradiol modulatory action on endogenous neurogenesis, synaptic plasticity, and cognitive function in AD.
阿尔茨海默病(AD)是一种认知和记忆障碍疾病,具有性别相关的流行病学特征,女性患者比男性多两倍。有新的证据表明,海马神经发生的改变发生在 AD 的早期阶段。在过去几十年中,人们广泛研究了可能有效减缓、阻止或再生 AD 中死亡神经元的治疗方法,但尚未发现有效的方法。调节内源性神经发生是 AD 的主要治疗靶点之一。越来越多的证据表明,神经甾体雌激素(17β-雌二醇)在神经发生、神经元活性和 AD 的突触可塑性中发挥支持作用。这种作用可能为 AD 提供预防和/或治疗方法。本文讨论了雌激素对 AD 中内源性神经发生、突触可塑性和认知功能的潜在调节作用的分子机制。