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天然黄酮类化合物在治疗阿尔茨海默病中对β-位点淀粉样前体蛋白裂解酶1的抑制作用

Beta-site APP-cleaving Enzyme-1 Inhibitory Role of Natural Flavonoids in the Treatment of Alzheimer's Disease.

作者信息

Singh Sandeep, Kushwaha Virendra, Sisodia Shriram, Kumar Shivendra, Sahu Kantrol Kumar

机构信息

Institute of Pharmaceutical Research, GLA University, Mathura, U.P. India.

Department of Pharmacology, Rajiv Academy for Pharmacy, Mathura, U.P. India.

出版信息

Cent Nerv Syst Agents Med Chem. 2025;25(1):39-48. doi: 10.2174/0118715249315049240710063455.

Abstract

Alzheimer's Disease (AD) is a devastating neurological condition characterized by a progressive decline in cognitive function, including memory loss, reasoning difficulties, and disorientation. Its hallmark features include the formation of neurofibrillary tangles and neuritic plaques in the brain, disrupting normal neuronal function. Neurofibrillary tangles, composed of phosphorylated tau protein and neuritic plaques, containing amyloid-β protein (Aβ) aggregates, contribute to the degenerative process. The discovery of the beta-site amyloid precursor protein cleaving enzyme 1 (BACE1) in 1999 revolutionized our understanding of AD pathogenesis. BACE1 plays a crucial role in the production of Aβ, the toxic protein implicated in AD progression. Elevated levels of BACE1 have been observed in AD brains and bodily fluids, underscoring its significance in disease onset and progression. Despite setbacks in clinical trials of BACE1 inhibitors due to efficacy and safety concerns, targeting BACE1 remains a promising therapeutic strategy for early-stage AD. Natural flavonoids have emerged as potential BACE1 inhibitors, demonstrating the ability to reduce Aβ production in neuronal cells and inhibit BACE1 activity. In our review, we delve into the pathophysiology of AD, highlighting the central role of BACE1 in Aβ production and disease progression. We explore the therapeutic potential of BACE1 inhibitors, including natural flavonoids, in controlling AD symptoms. Additionally, we provide insights into ongoing clinical trials and available patents in this field, shedding light on future directions for AD treatment research.

摘要

阿尔茨海默病(AD)是一种毁灭性的神经疾病,其特征是认知功能逐渐衰退,包括记忆力丧失、推理困难和定向障碍。其标志性特征包括大脑中神经原纤维缠结和神经炎斑块的形成,扰乱正常的神经元功能。由磷酸化tau蛋白组成的神经原纤维缠结和含有淀粉样β蛋白(Aβ)聚集体的神经炎斑块,促成了退行性过程。1999年β-位点淀粉样前体蛋白裂解酶1(BACE1)的发现彻底改变了我们对AD发病机制的理解。BACE1在Aβ的产生中起关键作用,Aβ是一种与AD进展相关的有毒蛋白质。在AD患者的大脑和体液中已观察到BACE1水平升高,这突出了其在疾病发生和发展中的重要性。尽管由于疗效和安全性问题,BACE1抑制剂的临床试验遭遇挫折,但靶向BACE1仍然是早期AD的一种有前景的治疗策略。天然黄酮类化合物已成为潜在的BACE1抑制剂,显示出能够减少神经元细胞中Aβ的产生并抑制BACE1活性。在我们的综述中,我们深入探讨了AD的病理生理学,强调了BACE1在Aβ产生和疾病进展中的核心作用。我们探索了BACE1抑制剂(包括天然黄酮类化合物)在控制AD症状方面的治疗潜力。此外,我们提供了对该领域正在进行的临床试验和现有专利的见解,为AD治疗研究的未来方向提供了线索。

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