Yang Seung-Hoon
Department of Medical Biotechnology, College of Life Science and Biotechnology, Dongguk University, Goyang, Korea.
Int Neurourol J. 2019 Nov;23(Suppl 2):S54-62. doi: 10.5213/inj.1938184.092. Epub 2019 Nov 30.
Alzheimer disease (AD) is a neurodegenerative disorder characterized by the loss of neuronal cells and the progressive decline of cognitive function. The major pathological culprit of AD is aggregation of amyloid-β (Aβ) and hyperphosphorylation of tau, eventually leading to progressive neuronal cell death and brain atrophy. However, the detailed molecular and cellular mechanisms underlying AD development as a result of neuronal cell death are little known. Although several hypotheses have been proposed regarding the development of AD, increasingly many studies suggest that the pathological progress of AD is not restricted to neuronal components such as Aβ and tau, but is also closely related to inflammatory responses in the brain. Abnormalities of Aβ and tau cause activity of pattern recognition receptors on the brain's immune cells, including microglia and astrocytes, and trigger the innate immune system by releasing inflammatory mediators in the pathogenesis of AD. In this review, we present a basic overview of the current knowledge regarding inflammation and molecular mediators in the pathological progress of AD.
阿尔茨海默病（AD）是一种神经退行性疾病，其特征是神经元细胞丧失和认知功能逐渐衰退。AD的主要病理元凶是β-淀粉样蛋白（Aβ）的聚集和tau蛋白的过度磷酸化，最终导致神经元细胞进行性死亡和脑萎缩。然而，由于神经元细胞死亡导致AD发展的详细分子和细胞机制鲜为人知。尽管已经提出了几种关于AD发展的假说，但越来越多的研究表明，AD的病理进展不仅限于Aβ和tau等神经元成分，还与大脑中的炎症反应密切相关。Aβ和tau的异常会导致大脑免疫细胞（包括小胶质细胞和星形胶质细胞）上模式识别受体的激活，并通过在AD发病机制中释放炎症介质来触发先天免疫系统。在这篇综述中，我们概述了目前关于AD病理进展中炎症和分子介质的现有知识。
