Department of Medicinal Chemistry, National Institute of Pharmaceutical Education and Research-Raebareli, New Transit Campus, Bijnor-Sisendi Road, Sarojini Nagar, Near CRPF Base Camp, Lucknow (Uttar Pradesh), 226002, India.
Department of Pharmacology & Toxicology, National Institute of Pharmaceutical Education and Research-Raebareli, New Transit Campus, Bijnor-Sisendi Road, Sarojini Nagar, Near CRPF Base Camp, Lucknow (Uttar Pradesh), 226002, India.
Curr Neuropharmacol. 2022;20(6):1174-1193. doi: 10.2174/1570159X19666211201094031.
Alzheimer's disease (AD) is a chronic neurodegenerative disease with no specific disease-modifying treatment. β-secretase (BACE1) is considered the potential and rationale target because it is involved in the rate-limiting step, which produces toxic Aβ peptides that leads to deposits in the form of amyloid plaques extracellularly, resulting in AD.
This study aims to discuss the role and implications of BACE1 and its inhibitors in the management of AD.
We have searched and collected the relevant quality work from PubMed using the following keywords "BACE1", BACE2", "inhibitors", and "Alzheimer's disease". In addition, we included the work which discusses the role of BACE1 in AD and the recent work on its inhibitors.
In this review, we have discussed the importance of BACE1 in regulating AD progression and the current development of BACE1 inhibitors. However, the development of a BACE1 inhibitor is very challenging due to the large active site of BACE1. Nevertheless, some of the BACE1 inhibitors have managed to enter advanced phases of clinical trials, such as MK-8931 (Verubecestat), E2609 (Elenbecestat), AZD3293 (Lanabecestat), and JNJ-54861911 (Atabecestat). This review also sheds light on the prospect of BACE1 inhibitors as the most effective therapeutic approach in delaying or preventing AD progression.
BACE1 is involved in the progression of AD. The current ongoing or failed clinical trials may help understand the role of BACE1 inhibition in regulating the Aβ load and cognitive status of AD patients.
阿尔茨海默病（AD）是一种慢性神经退行性疾病，目前尚无特异性的疾病修饰治疗方法。β-分泌酶（BACE1）被认为是潜在的合理靶点，因为它参与限速步骤，产生有毒的 Aβ肽，导致细胞外淀粉样斑块沉积，从而导致 AD。
本研究旨在讨论 BACE1 及其抑制剂在 AD 管理中的作用和意义。
我们使用以下关键词在 PubMed 上搜索和收集了相关的高质量文献：“BACE1”、“BACE2”、“抑制剂”和“阿尔茨海默病”。此外，我们还包括了讨论 BACE1 在 AD 中的作用以及其抑制剂的最新研究工作。
在本综述中，我们讨论了 BACE1 在调节 AD 进展中的重要性以及 BACE1 抑制剂的最新发展。然而，由于 BACE1 的活性部位较大，开发 BACE1 抑制剂极具挑战性。尽管如此，一些 BACE1 抑制剂已成功进入临床试验的后期阶段，如 MK-8931（Verubecestat）、E2609（Elenbecestat）、AZD3293（Lanabecestat）和 JNJ-54861911（Atabecestat）。本综述还阐明了 BACE1 抑制剂作为延迟或预防 AD 进展的最有效治疗方法的前景。
BACE1 参与 AD 的进展。目前正在进行或失败的临床试验可能有助于了解 BACE1 抑制在调节 AD 患者的 Aβ负荷和认知状态中的作用。
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