Neuroprotective, Anti-Inflammatory and Antifibrillogenic Offerings by Emodin against Alzheimer's Dementia: A Systematic Review

大黄素对阿尔茨海默病痴呆症的神经保护、抗炎和抗纤维化作用:系统评价

阅读:1

Abstract

Background: Alzheimer's disease (AD) is among the major causes of dementia in the elderly and exerts tremendous clinical, psychological and socio-economic constraints. Currently, there are no effective disease-modifying/retarding anti-AD agents. Emodin is a bioactive phytochemical with potent multimodal anti-inflammatory, antioxidant, and antifibrillogenic properties. In particular, emodin may result in significant repression of the pathogenic mechanisms underlying AD. The purpose of this review is to accumulate and summarize all the primary research data evaluating the therapeutic actions of emodin in AD pathogenesis. Methodology: The search, selection, and retrieval of pertinent primary research articles were systematically performed using a methodically designed approach. A variety of keyword combinations were employed on online scholarly web-databases. Strict preset inclusion and exclusion criteria were used to select the retrieved studies. Data from the individual studies were summarized and compiled into different sections, based upon their findings. Results: Cellular and animal research indicates that emodin exerts robust multimodal neuroprotection in AD. While emodin effectively prevents tau and amyloid-beta (Aβ) oligomerization, it also mitigates their neurotoxicity by attenuating neuroinflammatory, oxidative, and bioenergetic defects. Evidences for emodin-mediated enhancements in memory, learning, and cognition were also found in the literature. Conclusion: Emodin is a potential anti-AD dietary supplement; however, further studies are warrantied to thoroughly understand its target players and mechanisms. Moreover, human clinical data on emodin-mediated amelioration of AD phenotype is largely lacking, and must be addressed in the future. Lastly, the safety of exogenously supplemented emodin must be thoroughly evaluated.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。