肠道微生物组合成重要的核心代谢物,以防止认知能力下降,减轻阿尔茨海默病的发病和进展。

IF 2.8 Q2 NEUROSCIENCES
Journal of Alzheimer's disease reports Pub Date : 2024-12-23 eCollection Date: 2024-01-01 DOI:10.1177/25424823241309024
Nouf S Al-Abbas, Nehad A Shaer
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引用次数: 0

摘要

背景:本研究探讨肠道细菌代谢产生的肠道代谢物如何影响阿尔茨海默病(AD)等神经系统疾病。琥珀酸和短链脂肪酸等关键代谢物通过自主神经系统发出信号,并可穿过血脑屏障,影响中枢神经系统功能。目的:目的是研究肠道菌群在补偿AD代谢缺陷中的作用。通过分析野生型(WT)和APP/PS1小鼠,该研究探讨了微生物组如何影响关键代谢过程以及它是否可以减缓AD的进展。方法:对APP/PS1转基因AD模型小鼠和年龄匹配的WT C57BL/6雄性小鼠肠道微生物组的高通量测序数据进行微生物和代谢物谱分析。结果:α和β多样性分析显示各组间微生物组成存在差异。偏最小二乘判别分析和Anosim证实了WT和APP/PS1小鼠不同的微生物组谱。在属水平上,WT小鼠中以Vescimonas较多,APP/PS1小鼠中以Odoribacter、Lacrimispora、Helicobacter、Bacteroides和Alloprevotella较多。结论:虽然分类学上的差异没有直接将特定微生物与AD联系起来,但功能分析确定了关键代谢物-乙酰辅酶a,葡萄糖,琥珀酸盐,脂质,胆碱和乙酰胆碱-可能减轻能量不足和突触功能障碍。这项研究表明,微生物组可能有助于补偿与ad相关的损伤,为基于微生物组的治疗开辟了道路。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Gut microbiome synthesizes important core metabolites to prevent cognitive decline and mitigate onset and progression of Alzheimer's disease.

Background: This study explores how gut metabolites, produced through bacterial metabolism in the gut, influence neurological conditions like Alzheimer's disease (AD). Key metabolites such as succinate and short-chain fatty acids signal through the autonomic nervous system and can cross the blood-brain barrier, impacting central nervous system functions.

Objective: The aim is to examine the role of the gut microbiota in compensating for metabolic deficiencies in AD. By analyzing wild-type (WT) and APP/PS1 mice, the study investigates how the microbiome affects key metabolic processes and whether it can slow AD progression.

Methods: High-throughput sequencing data from the gut microbiomes of APP/PS1 transgenic AD model mice and age-matched WT C57BL/6 male mice were analyzed for microbial and metabolite profiles.

Results: Alpha and beta diversity analyses showed differences in microbial composition between groups. Partial least squares discriminant analysis and Anosim confirmed distinct microbiome profiles in WT and APP/PS1 mice. At the genus level, Vescimonas was more abundant in WT mice, while Odoribacter, Lacrimispora, Helicobacter, Bacteroides, and Alloprevotella were more prevalent in APP/PS1 mice.

Conclusions: While taxonomic differences did not directly link specific microorganisms to AD, functional analysis identified key metabolites-acetyl-CoA, glucose, succinate, lipids, choline, and acetylcholine-that may alleviate energy deficits and synaptic dysfunction. This study suggests that the microbiome may help compensate for AD-related impairments, opening avenues for microbiome-based therapies.

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