Age-related cognitive decline is primarily attributed to the progressive weakening of synaptic function and loss of synapses, while age-related gut microbial dysbiosis is known to impair synaptic plasticity and cognitive behavior by metabolic alterations. To improve the health of the elderly, the protective mechanisms of Oudemansiella raphanipes polysaccharide (ORP-1) against age-related cognitive decline are investigated. The results demonstrate that ORP-1 and its gut microbiota-derived metabolites SCFAs restore a healthy gut microbial population to handle age-related gut microbiota dysbiosis mainly by increasing the abundance of beneficial bacteria Dubosiella, Clostridiales, and Prevotellaceae and reducing the abundance of harmful bacteria Desulfovibrio, strengthen intestinal barrier integrity by abolishing age-related alterations of tight junction (TJ) and mucin 2 (MUC2) proteins expression, diminish age-dependent increase in circulating inflammatory factors, ameliorate cognitive decline by reversing memory- and synaptic plasticity-related proteins levels, and restrain hyperactivation of microglia-mediated synapse engulfment and neuroinflammation. These findings expand the understanding of prebiotic–microbiota–host interactions.

中文翻译：

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从 Oudemansiella raphanipes 分离的多糖 ORP-1 通过微生物群-肠-脑轴对抗年龄相关认知衰退的保护机制

与年龄相关的认知能力下降主要归因于突触功能的逐渐减弱和突触的丧失，而与年龄相关的肠道微生物失调会通过代谢改变损害突触可塑性和认知行为。为了改善老年人的健康，我们研究了萝卜多糖（ORP-1）对与年龄相关的认知衰退的保护机制。结果表明，ORP-1 及其肠道微生物衍生的代谢物 SCFA 主要通过增加有益细菌Dubosiella、Clostridiales和Prevotellaceae的丰度并减少有害细菌的丰度来恢复健康的肠道微生物种群，以应对与年龄相关的肠道微生物群失调。 Desulfovibrio，通过消除与年龄相关的紧密连接 (TJ) 和粘蛋白 2 (MUC2) 蛋白表达的改变来增强肠道屏障完整性，减少循环炎症因子的年龄依赖性增加，通过逆转记忆和突触可塑性相关蛋白来改善认知能力下降水平，并抑制小胶质细胞介导的突触吞噬和神经炎症的过度激活。这些发现扩展了对益生元-微生物群-宿主相互作用的理解。