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益智药物()对阿尔茨海默病的神经认知作用。

Neurocognitive Effect of Nootropic Drug () in Alzheimer's Disease.

作者信息

Chaudhari Kaustubh S, Tiwari Nishant R, Tiwari Rakesh R, Sharma Rohan S

机构信息

Department of Neurology, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA.

Department of Internal Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA.

出版信息

Ann Neurosci. 2017 May;24(2):111-122. doi: 10.1159/000475900. Epub 2017 May 12.

Abstract

Alzheimer's disease (AD) is a progressive neurodegenerative disease of the elderly. The rapid increase in its incidence has necessitated development of newer drugs. Ayurvedic herbal medications are increasingly researched due to their biosafety profile and usefulness in cognitive impairment. In this article, we critically reviewed one such (nootropic drug) -derived from extract of (EBm). Studies have shown that EBm promotes free radical scavenger mechanisms and protects cells in prefrontal cortex, hippocampus, and striatum against cytotoxicity and DNA damage implicated in AD. It also reduces lipoxygenase activity reducing lipid peroxidation, increases glutathione peroxidase and chelates iron. Administration of EBm was seen to protect the cholinergic neurons and reduce anticholinesterase activity comparable to donepezil, rivastigmine, and galantamine. It also reduces hippocampal β-amyloid deposition and stress-induced hippocampal damage. The neuroprotective effect of EBm is also due to nitric oxide-mediated cerebral vasodilation. EBm improved the total memory score and maximum improvement was seen in logical memory and paired associate learning in humans and reversed phenytoin-induced memory impairment in experimental model. EBm has not shown any serious clinical, neurological, hematological complications, or vital organs damage in experimental studies. Rats showed marked reduction in fertility; however, libido was unaffected. There is no experimental evidence of genotoxicity or teratogenesis by use of EBm. Mild nausea and gastrointestinal upset are seen in humans. promises to be a novel agent in AD; however, further human trials are recommended to verify the efficacy and rule out any side effects as evidenced by the experimental models.

摘要

阿尔茨海默病(AD)是一种老年人的进行性神经退行性疾病。其发病率的迅速上升使得开发更新的药物成为必要。阿育吠陀草药因其生物安全性和对认知障碍的有效性而受到越来越多的研究。在本文中,我们对一种从(EBm)提取物中衍生的(促智药)进行了批判性综述。研究表明,EBm促进自由基清除机制,并保护前额叶皮质、海马体和纹状体中的细胞免受与AD相关的细胞毒性和DNA损伤。它还降低脂氧合酶活性,减少脂质过氧化,增加谷胱甘肽过氧化物酶并螯合铁。与多奈哌齐、卡巴拉汀和加兰他敏相比,EBm的给药可保护胆碱能神经元并降低抗胆碱酯酶活性。它还减少海马体β-淀粉样蛋白沉积和应激诱导的海马体损伤。EBm的神经保护作用还归因于一氧化氮介导的脑血管舒张。EBm提高了总记忆评分,在人类的逻辑记忆和配对联想学习中观察到最大改善,并逆转了实验模型中苯妥英钠诱导的记忆障碍。在实验研究中,EBm未显示出任何严重的临床、神经学、血液学并发症或重要器官损伤。大鼠的生育力显著降低;然而,性欲未受影响。没有实验证据表明使用EBm会产生遗传毒性或致畸作用。在人类中可见轻度恶心和胃肠道不适。EBm有望成为AD的新型药物;然而,建议进行进一步的人体试验以验证疗效并排除实验模型所证明的任何副作用。

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