PDF(Pubmed)
Abstract：
Alzheimer\'s disease (AD) is a neurodegenerative process responsible for almost 70% of all cases of dementia. The clinical signs consist in progressive and irreversible loss of memory, cognitive, and behavioral functions. The main histopathological hallmark is the accumulation of amyloid-ß (Aß) peptide fibrils in the brain. To date, the origin of Aß has not been determined. Recent studies have shown that the gut microbiota produces Aß, and dysbiotic states have been identified in AD patients and animal models of AD. Starting from the hypothesis that maintaining or restoring the microbiota\'s eubiosis is essential to control Aß\'s production and deposition in the brain, we used a mixture of probiotics and prebiotics (symbiotic) to treat APPPS1 male and female mice, an animal model of AD, from 2 to 8 months of age and evaluated their cognitive performances, mucus secretion, Aβ serum concentration, and microbiota composition. The results showed that the treatment was able to prevent the memory deficits, the reduced mucus secretion, the increased Aβ blood levels, and the imbalance in the gut microbiota found in APPPS1 mice. The present study demonstrates that the gut-brain axis plays a critical role in the genesis of cognitive impairment, and that modulation of the gut microbiota can ameliorate AD\'s symptomatology.
摘要：
阿尔茨海默病（AD）是一种神经退行性过程，几乎占所有痴呆症病例的70％。临床症状包括进行性和不可逆转的记忆丧失，认知，和行为功能。主要的组织病理学标志是大脑中淀粉样蛋白β（Aβ）肽原纤维的积累。迄今为止,Aβ的起源尚未确定。最近的研究表明，肠道微生物群产生Aβ，已经在AD患者和AD动物模型中鉴定出生态失调状态。从维持或恢复微生物群的优生对控制大脑中Aβ的产生和沉积至关重要的假设开始，我们使用益生菌和益生元（共生）的混合物来治疗APPPS1雄性和雌性小鼠，AD的动物模型,从2到8个月的年龄，并评估他们的认知表现，粘液分泌，Aβ血清浓度,和微生物群组成。结果表明，该治疗能够防止记忆缺陷，粘液分泌减少，Aβ血液水平升高，以及在APPPS1小鼠中发现的肠道微生物群的不平衡。本研究表明，肠-脑轴在认知障碍的发生中起着至关重要的作用，肠道微生物群的调节可以改善AD的症状。
