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<p>This systematic review aims to identify microbial species associated with Alzheimer’s disease and clarify how they influence Alzheimer’s disease pathology, including immune system interactions and blood–brain barrier integrity. Following Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines, 18 studies were analyzed, revealing significant differences in gut microbiota composition between patients with Alzheimer’s disease and controls. Key findings include reduced beneficial bacteria, such as <i>Faecalibacterium prausnitzii</i> and <i>Roseburia hominis</i> and increased pro-inflammatory species like <i>Escherichia coli</i>. Mechanistically, <i>Escherichia coli</i> produces lipopolysaccharides, triggering the release of pro-inflammatory cytokines such as tumor necrosis factor-alpha. This response correlates with elevated YKL-40 levels and reduced beneficial bacteria like <i>Turicibacter</i>. Additionally, reductions in butyrate-producing bacteria impair blood–brain barrier integrity, while bile acid metabolism disruptions impair signaling pathways, exacerbating amyloid-beta aggregation. These findings highlight the interplay between gut microbiota-derived metabolites and neuroinflammation, suggesting that targeting the gut microbiota for novel diagnostic and therapeutic approaches in Alzheimer’s disease.</p>

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Gut Microbiota Dysbiosis and Neuroinflammation in Alzheimer’s Disease: a Systematic Review of Mechanistic Insights

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年1月1日

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  • Sofia Katsigianni,
  • Effrosyni Koutsouraki

摘要

This systematic review aims to identify microbial species associated with Alzheimer’s disease and clarify how they influence Alzheimer’s disease pathology, including immune system interactions and blood–brain barrier integrity. Following Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines, 18 studies were analyzed, revealing significant differences in gut microbiota composition between patients with Alzheimer’s disease and controls. Key findings include reduced beneficial bacteria, such as Faecalibacterium prausnitzii and Roseburia hominis and increased pro-inflammatory species like Escherichia coli. Mechanistically, Escherichia coli produces lipopolysaccharides, triggering the release of pro-inflammatory cytokines such as tumor necrosis factor-alpha. This response correlates with elevated YKL-40 levels and reduced beneficial bacteria like Turicibacter. Additionally, reductions in butyrate-producing bacteria impair blood–brain barrier integrity, while bile acid metabolism disruptions impair signaling pathways, exacerbating amyloid-beta aggregation. These findings highlight the interplay between gut microbiota-derived metabolites and neuroinflammation, suggesting that targeting the gut microbiota for novel diagnostic and therapeutic approaches in Alzheimer’s disease.