Gut dysbiosis induces PTSD-like behaviors via LPS-microglial activation; ACPC restores synaptic expression in mice
Gut microbiota dysbiosis promotes LPS-mediated microglial activation and PTSD-like behavior in mice, partially reversed by the herbal formulation ACPC.
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What the study showed
The abstract reports that gut dysbiosis upregulates LPS glycosylation precursor biosynthesis, driving non-C1q-dependent microglial activation and PTSD-like behaviors. ACPC, containing valerenal from Valerianae Jatamansi, reportedly restored synaptic proteins PSD95 and SYN1. FMT from PTSD mice was used to support a causal role of the microbiota.
How it was done
A PTSD mouse model was established via combined CF+SPS stress; behavioral outcomes were assessed by freezing, open-field, and elevated plus-maze tests. Antibiotic intervention, FMT, 16S rRNA sequencing, and metabolomics were applied.
Risk of bias
Exclusively preclinical; the abstract is truncated, preventing evaluation of quantitative results, sample sizes, and statistical analyses. The work is a preprint (SSRN 2026) without confirmed peer review.
What this study does NOT prove
This study does not prove that ACPC treats PTSD in humans or that the LPS-microglia axis is the dominant mechanism in human disease.
In clinical practice
No clinical application can be derived from this abstract. Animal model findings do not translate directly to human PTSD management.
Limitations
Exclusively preclinical; the abstract is truncated, preventing evaluation of quantitative results, sample sizes, and statistical analyses. The work is a preprint (SSRN 2026) without confirmed peer review.
Technical appendix
Version history
- 1.0 · 2026-08-27 — Auto-generated under Evidence Standard v1.0
Paid access: structured summary from public metadata; consult the original study at the source.
