Food research international (Ottawa, Ont.)Sep 3, 2026

How specific forms of quercetin affect the gut-brain system to protect against memory loss linked to colon inflammation

Gut-Brain Axis Weekly Brief ↗PubMed ↗DOI ↗

Updated Sep 4, 2026

Abstract

Quercetin glycosides improved cognitive deficits in mice with colitis, with specific sugar moieties influencing their effectiveness.

Four quercetin glycosides were evaluated for their effects on cognitive dysfunction associated with colitis.
All glycosides improved cognitive deficits and intestinal inflammation, but their efficacy varied based on the sugar structure.
Gal and Glc-Rha demonstrated the strongest effects on repairing the intestinal barrier and reducing neuroinflammation.
The glycosides modified gut microbiota composition, with Gal enriching Dubosiella and the other monoglycosides increasing Bifidobacterium.
These compounds inhibited the activation of a specific enzyme involved in the metabolism of tryptophan, which could prevent the production of neurotoxic metabolites.

Simplified

Inflammatory bowel disease is increasingly linked to cognitive impairment. Although quercetin glycosides are known to modulate intestinal homeostasis and gut-brain interactions, their specific impact on colitis-associated cognitive dysfunction and the underlying mechanisms remain poorly understood. This study evaluated the protective effects of four quercetin glycosides (hyperoside, Gal; isoquercitrin, Glc; quercitrin, Rha; rutin, Glc-Rha) in DSS-induced colitis mice. All glycoside supplementation effectively improved the cognitive deficits and intestinal inflammation, though efficacy depended on the specific sugar moiety. Gal and Glc-Rha exhibited the most pronounced effects in repairing the intestinal barrier, suppressing neuroinflammation, and restoring synaptic proteins, whereas Rha showed limited efficacy. Mechanistically, the glycosides selectively remodeled the gut microbiota (e.g., Dubosiella enriched by Gal and Bifidobacterium by three monoglycosides) and averted the aberrant activation of indoleamine 2,3-dioxygenase 1 in both the colon and brain. This suppression halted the pathological shift of tryptophan metabolism toward the neurotoxic kynurenine pathway, thereby preserving serotonin and indole pools. Consequently, this precise metabolic modulation correlated with reduced systemic endotoxemia, suppressed glial activation. Distinct glycosylation forms drive multi-target mechanisms along the gut-brain axis, providing new insights into targeted nutritional interventions to prevent IBD-related cognitive impairment.

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How specific forms of quercetin affect the gut-brain system to protect against memory loss linked to colon inflammation

Abstract

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