ArticleMicrobiome2026
Inulin alleviates vascular cognitive impairment by restoring prefrontal GABAergic function via microbiota-SCFA-GPR41/43 axis.
Article in Microbiome, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundVascular cognitive impairment (VCI) impairs medial prefrontal cortex (mPFC) function, a cognitive hub reliant on intact GABAergic transmission. Although prebiotics may counteract VCI by remodeling the gut microbiota, the underlying mechanisms remain unclear. This study investigated whether the prebiotic inulin could improve VCI by restoring mPFC GABAergic function via the gut-brain axis.
resultsIn a mouse model of VCI induced by bilateral carotid artery stenosis (BCAS), inulin supplementation ameliorated cognitive deficits and anxiety-like behaviors and reshaped the gut microbiota, particularly enriching SCFA-producing genera such as Ruminococcaceae. Antibiotic depletion abolished inulin's cognitive and intestinal barrier benefits, confirming microbiota dependence. In the mPFC, inulin reversed VCI-induced reductions in GABAergic synaptic transmission and GABA levels, which positively correlated with elevated colon short-chain fatty acid (SCFA) levels. Mechanistically, these effects were linked to the upregulation of SCFA receptors GPR41/43 and presynaptic restoration. Critically, shRNA-mediated knockdown of GPR41/43 abolished the behavioral and GABAergic benefits of SCFA supplementation, confirming the necessity of this signaling axis. Furthermore, to show the role of GABAergic function as inulin's final common pathway, pharmacological blockade of GABAergic signaling with bicuculline eliminated inulin's cognitive and anti-inflammatory benefits.
conclusionInulin alleviates VCI by elevating gut-derived SCFAs, which activate neuronal GPR41/43 in the mPFC to restore GABAergic function. These findings delineate a clear gut-mPFC pathway and support the therapeutic potential of inulin as an intervention targeting the microbiota-SCFA-GABA axis in cognitive disorders. Video Abstract.
Indexed as
Identifiers
42458594What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.