摘要
背景:最近的大多数报道表明,炎症介质在阿尔茨海默病(AD)的发病机制中起着核心作用,并且导致慢性低度炎症如压力,抑郁,肥胖和代谢综合征的病症增加发展为轻度认知功能障碍(MCI)和AD的几率。小胶质细胞是AD过程中的主要参与者:来自微环境的刺激可以诱导小胶质细胞转变为经典活化的炎症表型M1,或者与以不同类型的细胞因子分泌为特征的可选活化的M2表型相反。目前正在进行许多尝试以通过减少该疾病的炎症机制来延迟AD的进展。几项研究支持神经炎症与营养素,食物或饮食模式之间的关系,同时考虑到营养素之间的协同或拮抗生物化学相互作用以及相同营养素的不同食物来源。已经显示在植物食品中发现的天然抗氧化剂和抗炎化合物(例如水果,特别是浆果(例如草莓,蓝莓,黑醋栗,黑莓,蓝莓和桑)))发挥神经保护活性。目前还不清楚膳食生物活性化合物是否进入血脑屏障(BBB),对小胶质细胞和/或其他中枢神经系统(CNS)细胞发挥直接的抗炎或促炎作用。另一个假设是它们可能引发间接诱发中枢神经系统反应的外周反应。随后细胞因子的合成可能通过不同方式驱动小胶质细胞极化。因此,通过间接途径小胶质细胞检测并响应免疫脑信号。 结论:本综述总结了目前关于饮食,神经炎症和AD之间相互作用潜在机制的证据。
关键词: 阿尔茨海默病,营养性炎症,细胞因子,多酚,脂肪酸,中枢神经系统
Current Alzheimer Research
Title:Modulation of Inflammation as a Way of Delaying Alzheimer's Disease Progression: The Diet's Role
Volume: 15 Issue: 4
关键词: 阿尔茨海默病,营养性炎症,细胞因子,多酚,脂肪酸,中枢神经系统
摘要: Background: Most of the recent reports suggest that inflammatory mediators play a central role in the etiopathogenesis of Alzheimer's disease (AD) and that the conditions leading to a chronic low-grade inflammation, such as stress, depression, obesity and metabolic syndrome, increase the odds of developing Mild Cognitive Impairment (MCI) and AD. Microglia cells are the main actors in the AD process: stimuli from the microenvironment may induce microglia cells to switch to a classically activated inflammatory phenotype M1, or, on the contrary to an alternatively activated M2 phenotype characterized by the secretion of different types of cytokines. Many attempts are currently being made in order to delay the progression of AD by reducing inflammatory mechanisms underlying the disease. Several studies support a relationship among neuroinflammation and nutrients, foods or dietary patterns, taking into account the synergistic or antagonistic biochemical interactions among nutrients as well as the different food sources of the same nutrient. Natural antioxidant and anti-inflammatory compounds found in plant foods, such as fruits, particularly berries (such as strawberry, blueberry, blackcurrant, blackberry, blueberry and mulberry) have been shown to exert neuroprotective activity. It is still unclear whether the dietary bioactive compounds enter the Blood Brain Barrier (BBB) playing a direct antiinflammatory or pro-inflammatory effect on microglia and/or other Central Nervous System (CNS) cells. Another hypothesis is that they may trigger a peripheral reaction that induce indirectly a CNS' response. The subsequent synthesis of cytokines may drive microglia polarization by different ways. So, via an indirect route microglia detects and responds to immune-to-brain signaling.
Conclusion: This review summarizes current evidence about the potential mechanisms of the interaction among diet, neuroinflammation and AD.
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Cite this article as:
Modulation of Inflammation as a Way of Delaying Alzheimer's Disease Progression: The Diet's Role, Current Alzheimer Research 2018; 15 (4) . https://dx.doi.org/10.2174/1567205014666170829100100
DOI https://dx.doi.org/10.2174/1567205014666170829100100 |
Print ISSN 1567-2050 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5828 |
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