Alzheimer’s disease is a neurodegenerative disease characterized by progressive cognitive impairment. One of the primary reasons for the significant challenges in its clinical management is that the pathogenesis of Alzheimer’s disease has not been fully elucidated and effective intervention methods remain lacking. Therefore, it is crucial to explore relevant peripheral risk factors and novel therapeutic targets. The gut–microbiota–brain axis is a complex bidirectional regulatory network that integrates neural, endocrine, immune, and metabolic pathways. As the core of this axis, the gut microbiota modulates neuroinflammation, synaptic plasticity, and protein homeostasis. Specifically, metabolites such as short-chain fatty acids can cross the blood–brain barrier to regulate microglia activation, while microbial-mediated immunomodulatory effects directly influence the deposition of amyloid-β and the phosphorylation of tau protein. Existing studies have confirmed that Alzheimer’s disease patients exhibit gut microbiota imbalance, typically manifested as a decreased abundance of beneficial bacteria and the proliferation of potential proinflammatory bacteria. The dysbiosis is closely related to the accumulation of core pathological markers and the severity of cognitive impairment. This article aims to elucidate the interaction and underlying mechanisms between the gut microbiota and Alzheimer’s disease, offering an integrated analysis and research prospects to facilitate the development of novel intervention strategies.
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Zhu et al. (2026) studied this question.
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