Association of gut microbiota composition and function with a senescence-accelerated mouse model of Alzheimer's Disease using 16S rRNA gene and metagenomic sequencing analysis

Association of gut microbiota composition and function with a senescence-accelerated mouse model of Alzheimer's Disease using 16S rRNA gene and metagenomic sequencing analysis
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使用 16S rRNA 基因和宏基因组测序分析肠道微生物群组成和功能与衰老加速的阿尔茨海默病小鼠模型的关联

DOI:
10.18632/aging.101693
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发表时间:
2018-12-01
期刊:
影响因子:
5.2
通讯作者:
Zhang, Chunhu
Zhang, Chunhu
中科院分区:
医学2区
文献类型:
--
作者:
Peng, Weijun;Yi, Pengji;Zhang, Chunhu

文献摘要

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尽管肠道微生物群与阿尔茨海默病(AD)的潜在关联引起了人们的兴趣,但很少有研究直接评估这种关系或潜在机制。本研究采用16S rRNA基因和宏基因组测序方法,比较了衰老加速小鼠易感8 (SAMP8)和对照衰老加速小鼠耐药1 (SAMR1)的肠道菌群组成和功能分化。具体来说,16S测序结果显示,SAMP8小鼠的肠道微生物组的特征组成明显不同于SAMR1小鼠。此外,网络分析显示,SAMP8小鼠肠道微生物群的相关密度和操作分类单位的聚类降低。宏基因组结果显示,SAMP8小鼠中与这些变化相关的主要同源群功能分类簇是代谢簇。京都基因与基因组百科全书(KEGG)注释进一步证明了SAMP8小鼠中一些显性代谢相关的KEGG通路的相对丰度富集,与所提出的AD致病机制一致。总之,本研究提示肠道菌群组成和功能宏基因组的紊乱可能与AD有关。需要进一步的研究来阐明促进AD进展的潜在新机制。
Although an intriguing potential association of the gut microbiome with Alzheimer's disease (AD) has attracted recent interest, few studies have directly assessed this relationship or underlying mechanism. Here, we compared the gut microbiota composition and functional differentiation of senescence-accelerated mouse prone 8 (SAMP8) mice with control senescence-accelerated mouse resistant 1 (SAMR1) mice using 16S rRNA gene and metagenomic sequencing analysis, respectively. Specifically, 16S sequencing results showed that the SAMP8 mice displayed a characteristic composition of the gut microbiome that clearly differed from that of the SAMR1 mice. Moreover, network analysis revealed that the gut microbiota of SAMP8 mice had decreased correlation density and clustering of operational taxonomic units. Metagenomic results revealed that the predominant Cluster of Orthologous Groups functional category related to these changes was the metabolism cluster in SAMP8 mice. The Kyoto Encyclopedia of Genes and Genomes (KEGG) annotation further demonstrated enrichment of the relative abundance of some dominant metabolism-related KEGG pathways in the SAMP8 mice, consistent with the suggested pathogenic mechanisms of AD. In conclusion, this study suggests that perturbations of the gut microbiota composition and the functional metagenome may be associated with AD. Further studies are warranted to elucidate the potential new mechanism contributing to AD progression.