Businaro R, Corsi M, Asprino R, Di Lorenzo C, Laskin D, Corbo R M, Ricci S, Pinto A
Department of Medico-Surgical Sciences and Biotechnologies, Sapienza University of Rome, Rome, Italy.
Department of Experimental Medicine, Medical Physiopathology, Food Science and Endocrinology Section, Sapienza University of Rome, Rome, Italy.
Curr Alzheimer Res. 2018 Feb 22;15(4):363-380. doi: 10.2174/1567205014666170829100100.
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.
This review summarizes current evidence about the potential mechanisms of the interaction among diet, neuroinflammation and AD.
最近的大多数报告表明，炎症介质在阿尔茨海默病（AD）的病因发病机制中起核心作用，并且导致慢性低度炎症的状况，如压力、抑郁、肥胖和代谢综合征，会增加发生轻度认知障碍（MCI）和AD的几率。小胶质细胞是AD进程中的主要参与者：来自微环境的刺激可能诱导小胶质细胞转变为经典激活的炎症表型M1，或者相反，转变为以分泌不同类型细胞因子为特征的替代激活的M2表型。目前正在进行许多尝试，以通过减少该疾病潜在的炎症机制来延缓AD的进展。考虑到营养素之间的协同或拮抗生化相互作用以及同一营养素的不同食物来源，多项研究支持神经炎症与营养素、食物或饮食模式之间存在关联。植物性食物中发现的天然抗氧化和抗炎化合物，如水果，特别是浆果（如草莓、蓝莓、黑加仑、黑莓、越橘和桑椹）已显示出具有神经保护活性。目前尚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）细胞产生直接的抗炎或促炎作用。另一种假设是它们可能引发外周反应，间接诱导中枢神经系统的反应。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，小胶质细胞通过间接途径检测并响应免疫-脑信号。
本综述总结了关于饮食、神经炎症和AD之间相互作用潜在机制的当前证据。
