阿尔茨海默症(Alzheimer’s disease，AD)是一种进行性中枢神经系统退行性疾病。在临床上表现为认知和记忆功能下降，以神经元细胞内的神经纤维缠结和细胞外的老年斑为主要病理特征。目前，关于AD发病机制存在多种假说，如β-淀粉样肽(amyloid-β peptide，Aβ)级联假说、Tau蛋白异常磷酸化假说、胆碱能假说、氧化应激假说等。茶叶中含有儿茶素、茶氨酸等天然活性成分，研究表明，茶叶活性成分能提供多靶标的AD保护作用，尤其是表没食子儿茶素没食子酸酯(epigallocatechin-3-gallate，EGCG)，可通过调节α、β、γ-分泌酶活性或蛋白激酶C等信号通路减少Aβ生成，抑制Aβ聚集或破坏纤维状Aβ，抑制Tau蛋白过度磷酸化，调节乙酰胆碱、谷氨酸神经递质水平，抗氧化应激等预防AD。为此，本文综述了AD主要发病机制以及近10年茶叶活性成分对AD的神经保护机理研究进展。

Alzheimer’s disease (AD) is a progressive neurodegenerative disorder of central nervous system. The clinical manifestations of this disease are the decline in cognitive capacity and memory, and the main pathological characteristics of AD are intracellular neurofibrillary tangles and extracellular senile plaque in neurons. At present, various hypotheses on the AD pathogenesis have been reported, such as amyloid-β peptide (Aβ) cascade hypothesis, Tau hyperphosphorylation hypothesis, cholinergic hypothesis, oxidative stress hypothesis, etc. Tea contains catechins, theanine, and other natural bioactive components. Previous studies have shown that the bioactive components of tea can provide multi-targeted neuroprotection in AD. Particularly through the regulation of α-, β-, and γ-secretase activities or protein kinase C and other signaling pathways, epigallocatechin-3-gallate (EGCG) can reduce the production of Aβ, prevent the aggregation of Aβ or disassemble the preformed Aβ fibrils, inhibit hyperphosphorylation of Tau protein, modulate levels of neurotransmitters (acetylcholine and glutamate), and increase the resistance to oxidative stress, thus preventing AD. The main findings on pathogeneses of AD and the research progress on the neuroprotective mechanisms of tea bioactive components in AD over the last decade are reviewed in this paper.

现代农业产业技术体系建设专项资金（CARS-23）