靶向血小板活化因子信号在神经退行性疾病中的治疗益处。

IF 3.3 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY
Theodora Adamantidi, Andreas M Grabrucker, Alexandros Tsoupras
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引用次数: 0

摘要

神经退行性疾病(NDs),包括痴呆、阿尔茨海默病(AD)和帕金森病(PD),是与年龄相关的疾病,与慢性炎症、氧化应激、基因突变、自身免疫源性炎症和其他外部危险因素密切相关。它们的特征是进行性神经元丧失、认知能力下降和/或运动功能障碍,慢性炎症是加剧NDs发生的关键因素。血小板活化因子(PAF)是连接炎症与NDs的最重要的分子炎症介质之一,它是调节神经炎症、细胞凋亡和神经元损伤的关键信号。PAF活性和代谢水平的失调及其受体(PAF- r)的过度表达与炎症反应加剧相关,进一步加重神经退行性变。这篇文章强调了PAF在神经退行性疾病中的作用,特别关注PAF抑制剂在预防和治疗神经退行性疾病方面的潜在医学应用的新见解。我们评估了最近提出的通过天然和/或合成抑制剂或两者结合靶向PAF信号通路的概念。它探索了这些抑制剂的潜力,可能通过抗炎、抗衰老、减缓疾病进展和保持认知和运动功能障碍,为NDs提供显著的预防和治疗益处。本文还讨论了这种治疗方法的现状和未来前景。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Targeting Platelet Activating Factor Signaling for Therapeutic Benefits in Neurodegenerative Disorders.

Neurodegenerative disorders (NDs), including dementia, Alzheimer's disease (AD), and Parkinson's disease (PD), are age-related diseases closely associated with chronic inflammation, oxidative stress, gene mutations, autoimmune-derived inflammation, and other external risk factors. They are characterized by progressive neuronal loss, cognitive decline, and/or motor dysfunction, with chronic inflammation being a key player in intensifying NDs' occurrence. One of the most important molecular inflammatory mediators linking inflammation to NDs is the platelet-activating factor (PAF) and its pivotal signaling for regulating neuroinflammation, apoptosis, and neuronal damage. Dysregulation of PAF activity and metabolism/levels, along with overexpression of its receptor (PAF-R) have been associated with exacerbated inflammatory responses, further aggravating neurodegeneration. This article highlights the role of PAF in neurodegeneration, with a particular focus on novel insights into the potential medicinal use of PAF inhibitors for the prevention and treatment of neurodegenerative diseases. We evaluate the recently proposed concept of targeting the PAF signaling pathway through either natural and/or synthetic inhibitors or a combination of both. It explores the potential of these inhibitors to offer significant preventative and therapeutic benefits against NDs, likely through anti-inflammatory anti-aging effects and by slowing down the disease progression and preserving cognitive and motor dysfunction. Current status and future perspectives of such therapeutic approaches are also discussed.

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