Alzheimer's disease (AD) is a chronic neurodegenerative disease characterized by the formation of intracellular neurofibrillary tangles (NFTs) and extracellular amyloid plaques. Growing evidence has suggested that AD pathogenesis is not only limited to the neuronal compartment but also strongly interacts with immunological processes in the brain. On the other hand, aggregated and misfolded proteins can bind with pattern recognition receptors located on astroglia and microglia and can, in turn, induce an innate immune response, characterized by the release of inflammatory mediators, ultimately playing a role in both the severity and the progression of the disease. It has been reported by genome-wide analysis that several genes which elevate the risk for sporadic AD encode for factors controlling the inflammatory response and glial clearance of misfolded proteins. Obesity and systemic inflammation are examples of external factors which may interfere with the immunological mechanisms of the brain and can induce disease progression. In this review, we discussed the mechanisms and essential role of inflammatory signaling pathways in AD pathogenesis. Indeed, interfering with immune processes and modulation of risk factors may lead to future therapeutic or preventive AD approaches.

中文翻译：

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阿尔茨海默病发病机制中的神经炎症信号传导。

阿尔茨海默病 (AD) 是一种慢性神经退行性疾病，其特征在于细胞内神经原纤维缠结 (NFT) 和细胞外淀粉样斑块的形成。越来越多的证据表明，AD 发病机制不仅限于神经元区室，而且与大脑中的免疫过程密切相关。另一方面，聚集和错误折叠的蛋白质可以与位于星形胶质细胞和小胶质细胞上的模式识别受体结合，进而诱导先天免疫反应，其特征是释放炎症介质，最终在严重程度和严重程度方面发挥作用。疾病的进展。据全基因组分析报道，提高散发性 AD 风险的几个基因编码控制炎症反应和错误折叠蛋白的神经胶质清除的因子。肥胖和全身炎症是外部因素的例子，它们可能会干扰大脑的免疫机制并可能导致疾病进展。在这篇综述中，我们讨论了炎症信号通路在 AD 发病机制中的机制和重要作用。事实上，干扰免疫过程和调节风险因素可能会导致未来的治疗或预防 AD 方法。我们讨论了炎症信号通路在 AD 发病机制中的机制和重要作用。事实上，干扰免疫过程和调节风险因素可能会导致未来的治疗或预防 AD 方法。我们讨论了炎症信号通路在 AD 发病机制中的机制和重要作用。事实上，干扰免疫过程和调节风险因素可能会导致未来的治疗或预防 AD 方法。