Lactobacillus plantarum DP189 prevents cognitive dysfunction in D-galactose/AlCl3 induced mouse model of Alzheimer's disease via modulating gut microbiota and PI3K/Akt/GSK-3 beta signaling pathway
文献类型： 外文期刊
作者： Song, Xinping 1 ; Zhao, Zijian 1 ; Zhao, Yujuan 1 ; Wang, Zhiguo 2 ; Wang, Chao 1 ; Yang, Ge 1 ; Li, Shengyu 1 ;
作者机构： 1.Jilin Acad Agr Sci, Inst Agrofood Technol, 1363 Sheng Tai St, Changchun 130033, Jilin, Peoples R China
2.Gen Hosp Northern Theater Command, Dept Nucl Med, Shenyang, Peoples R China
3.Yanbian Univ, Coll Agr, Yanji, Peoples R China
关键词： Lactobacillus plantarum; Alzheimer's disease; gut microbiota; GSK-3 beta; PI3K; microbiota-gut-brain axis; cognitive dysfunction; probiotics
期刊名称：NUTRITIONAL NEUROSCIENCE （ 影响因子：5.0； 五年影响因子：4.657 ）
ISSN： 1028-415X
年卷期：
页码：
收录情况： SCI
摘要： Probiotic intervention has beneficial effects on host brain function and behavior via regulating microbiota-gut-brain axis; however, the underlying mechanism is not yet understood. Herein, we investigated that the effects of Lactobacillus plantarum DP189 (DP189) administration in preventing cognitive dysfunction and pathology of Alzheimer's disease (AD) in D-galactose (D-gal) and AlCl3-induced AD model mice. After L. plantarum DP189 intervention for 10 weeks, we assessed cognitive behavior, neurotransmitter expression, histological changes, microbial communities, and the mechanisms underlying the disease in AD model mice. The results showed that L. plantarum DP189 intervention prevented cognitive dysfunction by behavioral test. Increased levels of serotonin, dopamine, and gamma-aminobutyric acid positively affected the pathological processes by ameliorating neuronal damage, beta-amyloid deposition, and tau pathology. L. plantarum DP189 intervention simultaneously modulated the gut microbial communities to alleviate gut dysbiosis. Moreover, L. plantarum DP189 inhibited tau hyperphosphorylation by regulating the PI3 K/Akt/GSK-3 beta pathway. These findings indicated that L. plantarum DP189 intervention is a promising therapeutic strategy to prevent the onset and development of AD.
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