Department of Clinical and Behavioural Neurology, Santa Lucia Foundation IRCCS, 00179 Rome, Italy.
Memory Clinic, Department of Systems Medicine, University of Tor Vergata, 00133 Rome, Italy.
Biomolecules. 2022 Aug 22;12(8):1161. doi: 10.3390/biom12081161.
Increasing evidence strongly supports the key role of neuroinflammation in the pathophysiology of neurodegenerative diseases, such as Alzheimer's disease, frontotemporal dementia, and amyotrophic lateral sclerosis. Neuroinflammation may alter synaptic transmission contributing to the progression of neurodegeneration, as largely documented in animal models and in patients' studies. In the last few years, palmitoylethanolamide (PEA), an endogenous lipid mediator, and its new composite, which is a formulation constituted of PEA and the well-recognized antioxidant flavonoid luteolin (Lut) subjected to an ultra-micronization process (co-ultraPEALut), has been identified as a potential therapeutic agent in different disorders by exerting potential beneficial effects on neurodegeneration and neuroinflammation by modulating synaptic transmission. In this review, we will show the potential therapeutic effects of PEA in animal models and in patients affected by neurodegenerative disorders.
越来越多的证据强烈支持神经炎症在神经退行性疾病（如阿尔茨海默病、额颞叶痴呆和肌萎缩侧索硬化症）的病理生理学中的关键作用。神经炎症可能会改变突触传递，从而促进神经退行性变的发展，这在动物模型和患者研究中得到了充分证实。在过去的几年中，内源性脂质介质棕榈酰乙醇酰胺（PEA）及其新型复合物，即通过超微化过程（co-ultraPEALut）构成的 PEA 和众所周知的抗氧化黄酮芦丁（Lut）的复合物，已被确定为一种潜在的治疗剂，可通过调节突触传递对神经退行性变和神经炎症产生潜在的有益作用，从而在不同疾病中发挥作用。在这篇综述中，我们将展示 PEA 在动物模型和受神经退行性疾病影响的患者中的潜在治疗效果。
