ReviewInternational journal of molecular sciences2026
Magnesium Status in Celiac Disease: Potential Links with Neuroinflammatory Pathways and Gut-Brain Axis Dysfunction.
Review in International journal of molecular sciences, 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
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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.
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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.
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Who cites it
0 citing papers in PubMed.
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Celiac disease (CD) is a chronic immune-mediated enteropathy characterized by intestinal inflammation, epithelial barrier dysfunction, and a wide range of extraintestinal manifestations, including neurological disorders. Magnesium (Mg) status has attracted increasing interest because Mg is involved in inflammatory regulation, oxidative balance, mitochondrial function, calcium homeostasis, and neuronal signaling, suggesting a potential role in neuroimmune pathways and gut-brain axis communication. This narrative review critically evaluates the available evidence regarding the relationship between Mg status, neuroinflammation, and gut-brain axis dysfunction in CD. A literature search was performed using PubMed, Scopus, and Web of Science, focusing primarily on studies published between 2019 and 2025, while earlier landmark publications were included to provide mechanistic context. The review was conducted according to the Scale for the Assessment of Narrative Review Articles (SANRA). Current evidence indicates that reduced Mg status in CD is primarily associated with intestinal malabsorption, chronic inflammation, and dietary inadequacies. Experimental and translational studies support several mechanisms through which Mg may influence neuroimmune signaling; however, clinical evidence directly linking altered Mg status to neurological manifestations in patients with CD remains limited. Overall, Mg should be regarded as a potential modifier of inflammatory and neuroimmune pathways rather than an independent pathogenic factor. Further prospective studies are needed to clarify the contribution of Mg homeostasis to neurological manifestations in CD.
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