ArticleBMC biology2025
Gut dysbiosis leads to cognitive decline through CNTF-mediated activation of microglia in mice.
Article in BMC biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Gut microbiota dysbiosis shapes brain T-cell immunity in accelerated aging.Gut microbes · 2026Article
- Germ-free piglets display variable neuroinflammatory-like perturbations in prefrontal cortical microglia.bioRxiv : the preprint server for biology · 2026Article
- The gut-brain axis: mechanisms linking intestinal dysbiosis with stroke.Frontiers in cell and developmental biology · 2026Review
- Gut-brain axis mechanisms of remote brain dysfunction after traumatic spinal cord injury: immune inflammation, the vagus nerve, and neuroendocrine pathways.Frontiers in cellular neuroscience · 2026Review
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Authors and funding
11 authors.
Funding
Abstract
backgroundThe gut microbiota is essential for maintaining host homeostasis through its influence on metabolism, immunity, and neural signalling. Disruption of this microbial balance, known as gut dysbiosis, can alter gut-brain communication and has been associated with cognitive decline, with impairments in learning and memory. However, the cellular and molecular factors that lead to cognitive decline are not well understood. In this study we used an antibiotic-induced gut dysbiosis model.
resultsWe observed that the animals with antibiotic-induced gut dysbiosis showed deficits in cognition, especially long-term memory consolidation. There was an increase in astrocytes and microglial activation in the CA1 subregion of the hippocampus. The microglia were observed to engage in synaptic pruning at the presynaptic terminals. This aberrant pruning might have disrupted synaptic plasticity and connectivity, contributing to the observed cognitive deficiency. CNTF was also observed to be elevated along with activation of the JAK/STAT3 pathway. CNTF can activate microglia. Our findings revealed that astrocytes, microglia, and CNTF form an inflammatory activation loop within the CA1 region of the hippocampus following antibiotic-induced gut dysbiosis.
conclusionsIn summary, our study demonstrates that antibiotic-induced gut dysbiosis triggers a cascade of neuroinflammatory events in the hippocampus, involving the elevation of CNTF, microglial pruning at presynaptic terminals, and reciprocal activation of glial cells, resulting in cognitive deficits. These findings highlight the critical role of gut-brain communication in maintaining neural homeostasis and identify CNTF as a potential therapeutic target for dysbiosis-associated cognitive disorders.
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