ArticleFrontiers in neuroscience2026
Moxa-combustion byproducts improve cognitive function via olfactory-mediated modulation of the GSK-3β/CREB pathway.
Article in Frontiers in neuroscience, 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
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: Olfactory dysfunction in early-stage Alzheimer's disease (AD) is associated with GSK-3β abnormalities localized in the olfactory bulb. These pathological changes not only compromise hippocampus-dependent learning and memory via synaptic impairments but also contribute to emotional disturbances such as anxiety and depression. Given that moxa-combustion byproducts (MCB), a key therapeutic component of moxibustion, enhance synaptic plasticity and improve cognition, this study aimed to investigate whether MCB ameliorates cognitive deficits by olfactory-mediated modulation of the GSK-3β/CREB pathway. Methods: Four-month-old APP/PS1 mice received 12-week MCB interventions. Behavioral assessments (Morris water maze, buried food pellet test and open field test) evaluated olfactory and cognitive functions. Pathological changes and synaptic structure in olfactory bulbs and hippocampus were analyzed via hematoxylin-eosin (HE) staining and transmission electron microscopy (TEM). Protein levels of GSK3β, CREB, and c-Fos were quantified by Western blot (WB). Results: MCB significantly improved spatial learning, memory, and olfactory performance in AD mice. HE staining showed that MCB increased the number of olfactory mitral cells and hippocampal CA1 neurons, and could regulate synaptic plasticity. MCB downregulated GSK-3β while upregulating CREB and c-Fos in both olfactory bulb and hippocampal tissues. The effect of MCB disappeared after olfactory blockade using 3-methylindole, suggesting olfactory-mediated action. Conclusion: MCB enhances cognitive-olfactory functions and mitigates anxiety- and depression-like behaviors in AD mice, potentially via modulation of GSK-3β/CREB pathway-related proteins in the olfactory system.
Indexed as
Identifiers
What Socratic 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 Socratic graph.