Department of Neonatology, Hospital Clínic-Maternitat, ICGON, BCNatal, 08028 Barcelona, Spain.
Institut de Recerca Sant Joan de Déu, 08950 Esplugues de Llobregat, Spain.
Nutrients. 2021 Jun 29;13(7):2232. doi: 10.3390/nu13072232.
In recent years, neurological and neurodegenerative disorders research has focused on altered molecular mechanisms in search of potential pharmacological targets, e.g., imbalances in mechanisms of response to oxidative stress, inflammation, apoptosis, autophagy, proliferation, differentiation, migration, and neuronal plasticity, which occur in less common neurological and neurodegenerative pathologies (Huntington disease, multiple sclerosis, fetal alcohol spectrum disorders, and Down syndrome). Here, we assess the effects of different catechins (particularly of epigalocatechin-3-gallate, EGCG) on these disorders, as well as their use in attenuating age-related cognitive decline in healthy individuals. Antioxidant and free radical scavenging properties of EGCG -due to their phenolic hydroxyl groups-, as well as its immunomodulatory, neuritogenic, and autophagic characteristics, makes this catechin a promising tool against neuroinflammation and microglia activation, common in these pathologies. Although EGCG promotes the inhibition of protein aggregation in experimental Huntington disease studies and improves the clinical severity in multiple sclerosis in animal models, its efficacy in humans remains controversial. EGCG may normalize DYRK1A (involved in neural plasticity) overproduction in Down syndrome, improving behavioral and neural phenotypes. In neurological pathologies caused by environmental agents, such as FASD, EGCG enhances antioxidant defense and regulates placental angiogenesis and neurodevelopmental processes. As demonstrated in animal models, catechins attenuate age-related cognitive decline, which results in improvements in long-term outcomes and working memory, reduction of hippocampal neuroinflammation, and enhancement of neuronal plasticity; however, further studies are needed. Catechins are valuable compounds for treating and preventing certain neurodegenerative and neurological diseases of genetic and environmental origin. However, the use of different doses of green tea extracts and EGCG makes it difficult to reach consistent conclusions for different populations.
近年来，神经和神经退行性疾病的研究集中在改变的分子机制上，以寻找潜在的药物靶点，例如氧化应激、炎症、细胞凋亡、自噬、增殖、分化、迁移和神经元可塑性反应机制的失衡，这些机制发生在不太常见的神经和神经退行性病理中（亨廷顿病、多发性硬化症、胎儿酒精谱系障碍和唐氏综合征）。在这里，我们评估了不同儿茶素（特别是表没食子儿茶素-3-没食子酸酯，EGCG）对这些疾病的影响，以及它们在减轻健康个体与年龄相关的认知衰退中的应用。由于 EGCG 的酚羟基，其具有抗氧化和自由基清除特性，以及其免疫调节、神经突生成和自噬特性，使这种儿茶素成为对抗神经炎症和小胶质细胞激活的有前途的工具，这些是这些病理中的常见现象。尽管 EGCG 促进了实验性亨廷顿病研究中蛋白质聚集的抑制，并改善了动物模型中多发性硬化症的临床严重程度，但它在人类中的疗效仍存在争议。EGCG 可能使唐氏综合征中涉及神经可塑性的 DYRK1A 过度产生正常化，从而改善行为和神经表型。在环境因素引起的神经病理学中，如 FASD，EGCG 增强抗氧化防御，调节胎盘血管生成和神经发育过程。正如在动物模型中所证明的，儿茶素减轻与年龄相关的认知衰退，从而改善长期结果和工作记忆，减少海马神经炎症，并增强神经元可塑性；然而，还需要进一步的研究。儿茶素是治疗和预防某些遗传和环境来源的神经退行性和神经疾病的有价值的化合物。然而，不同剂量的绿茶提取物和 EGCG 的使用使得难以对不同人群得出一致的结论。
